Polycystic ovary syndrome (PCOS) is a common female condition typified by reproductive, hyperandrogenic, and metabolic features. Polycystic ovary syndrome is a genetic condition, exacerbated by obesity. There is a close link between obesity and PCOS based on epidemiological data, and more recently corroborated through genetic studies. There are many mechanisms mediating the effects of weight-gain and obesity on the development of PCOS. The metabolic effects of insulin resistance and steroidogenic and reproductive effects of hyperinsulinaemia are important mechanisms. Adipokine production by subcutaneous and visceral fat appears to play a part in metabolic function. However, given the complexity of PCOS pathogenesis, it is important also to consider possible effects of PCOS on further weight-gain, or at least on hampering attempts at weight-loss and maintenance through lifestyle changes. Possible mediators of these effects include changes in energy expenditure, mental ill health, or physical inactivity. In this brief review, we discuss the main mechanisms that underlie the association between obesity and PCOS, from divergent perspectives of weight-gain contributing to development of PCOS and vice versa. We also consider novel management options for women with obesity and PCOS.

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Background: Diets have been a central component of lifestyle modification for decades. The Low-Carbohydrate Diet (LCD), originally conceived as a treatment strategy for intractable epilepsy (due to its association with ketogenesis), became popular in the 1970s and since then has risen to prominence as a weight loss strategy. Objective: To explore the efficacy, limitations and potential safety concerns of the LCD. Data Sources: We performed a narrative review, based on relevant articles written in English from a Pubmed search, using the terms ‘low carbohydrate diet and metabolic health’. Results: Evidence supports the efficacy of the LCD in the short-term (up to 6-months) for reduction in fat mass and remission of Type 2 Diabetes Mellitus (T2D). However, the longer-term efficacy of the LCD is disappointing, with diminishment of weight loss potential and metabolic benefits of the LCD beyond 6-months of its adoption. Furthermore, practical limitations of the LCD include the associated restriction of food choices that restrict the acceptability of the LCD for the individual, particularly over the longer term. There are also safety concerns of the LCD that stem from nutritional imbalances (with a relative excess of dietary fat and protein intake with associated dyslipidaemia and increased risk of insulin resistance and T2D development) and ketotic effects. Finally, the LCD often results in a reduction in dietary fibre intake, with potentially serious adverse consequences for overall health and the gut microbiota. Conclusions: Although widely adopted, the LCD usually has short-lived metabolic benefits, with limited efficacy and practicality over the longer term. Dietary modification needs tailoring to the individual, with careful a priori assessments of food preferences to ensure acceptability and adherence over the longer term, with avoidance of dietary imbalances and optimization of dietary fibre intake (primarily from plant-based fruit and vegetables), and with a posteriori assessments of the highly individual responses to the LCD. Finally, we need to change our view of diets from simply an excipient for weight loss to an essential component of a healthy lifestyle.

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Over unimaginable expanses of evolutionary time, our gut microbiota have co-evolved with us, creating a symbiotic relationship in which each is utterly dependent upon the other. Far from confined to the recesses of the alimentary tract, our gut microbiota engage in complex and bi-directional communication with their host, which have far-reaching implications for overall health, wellbeing and normal physiological functioning. Amongst such communication streams, the microbiota–gut–brain axis predominates. Numerous complex mechanisms involve direct effects of the microbiota, or indirect effects through the release and absorption of the metabolic by-products of the gut microbiota. Proposed mechanisms implicate mitochondrial function, the hypothalamus–pituitary–adrenal axis, and autonomic, neuro-humeral, entero-endocrine and immunomodulatory pathways. Furthermore, dietary composition influences the relative abundance of gut microbiota species. Recent human-based data reveal that dietary effects on the gut microbiota can occur rapidly, and that our gut microbiota reflect our diet at any given time, although much inter-individual variation pertains. Although most studies on the effects of dietary macronutrients on the gut microbiota report on associations with relative changes in the abundance of particular species of bacteria, in broad terms, our modern-day animal-based Westernized diets are relatively high in fats and proteins and impoverished in fibres. This creates a perfect storm within the gut in which dysbiosis promotes localized inflammation, enhanced gut wall permeability, increased production of lipopolysaccharides, chronic endotoxemia and a resultant low-grade systemic inflammatory milieu, a harbinger of metabolic dysfunction and many modern-day chronic illnesses. Research should further focus on the colony effects of the gut microbiota on health and wellbeing, and dysbiotic effects on pathogenic pathways. Finally, we should revise our view of the gut microbiota from that of a seething mass of microbes to one of organ-status, on which our health and wellbeing utterly depends. Future guidelines on lifestyle strategies for wellbeing should integrate advice on the optimal establishment and maintenance of a healthy gut microbiota through dietary and other means. Although we are what we eat, perhaps more importantly, we are what our gut microbiota thrive on and they thrive on what we eat.

Background Early career general practitioners are known to be at high risk of burnout. There is a need for widely applicable, cost-effective evidence-based interventions to develop trainees’ protective skills and strategies. Results Of 120 eligible trainees, 23 (19.2%) expressed interest in participating, 17 subsequently started the course, and 15 completed at least 5 out of its 6 sessions. All psychological measures were stable for the six-week period prior to commencing the course. Following the course, there were statistically significant (p < 0.05) improvements in wellbeing, resilience, mindfulness, emotional exhaustion, disengagement, and stress scores. Participants described numerous benefits, and most stated that they would recommend it to colleagues. Conclusion Including mindful practice within general practice vocational training is feasible, and in this study it benefited the psychological wellbeing of participants. Further research is needed to explore ways of increasing uptake and course completion, the sustainability of its effects, and the wider applicability of this approach.

To tackle the complexity of the global obesity epidemic, it is important to consider the many predisposing factors that underlie progressive and sustained weight gain. Some of the biological drivers for weight gain following initial weight loss include persistent changes in appetite hormones [including ghrelin and postprandial plasma peptide YY (PYY)], and ‘persistent metabolic adaptation’. However, many factors within our busy, stressful modern-day environment seem to conspire towards promotion of weight gain. These include the effects of sleep deprivation on appetite regulation, and the effects of modern-day technology on ‘attention competition’. These factors, combined with cultural and societal factors can result in a ‘mindless’ attitude regarding eating-related behaviour that is likely to predispose to weight gain. In addition to the external environment, our internal environment within the gut has also changed radically within the last few decades, resulting from changes in fibre intake, and increased ingestion of highly refined, sterilised and processed foods. Although contentious, these dietary changes have implications for our gut microbiota, and possible downstream effects on control of appetite and metabolism. In this brief review, we consider some of the novel predisposing factors for weight gain within our modern-day 21st century environments (both external and internal), and explore how legal terminology can help to conceptualise the numerous factors that contribute towards weight gain, and, ultimately the global obesity epidemic.

Background: Dietary sodium intake mismatches urinary sodium excretion over prolonged periods. Our aims were to localize and quantify electrostatically bound sodium within human skin using triple quantum filtered (TQF) protocols for magnetic resonance imaging (MRI) and spectroscopy (MRS), and explore dermal sodium in Type 2 Diabetes Mellitus (T2D). Methods:We recruited adult participants with T2D (n=9) and euglycemic participants with no history of Diabetes Mellitus (n=8). All had undergone lower limb amputations or abdominal skin reduction surgery for clinical purposes. We used 20m in-plane resolution 1 H MRI to visualise anatomical skin regions ex vivo from skin biopsies taken intra-operatively, 23 Na TQF MRI/MRS to explore distribution and quantification of freely dissolved and bound sodium and Inductively Coupled Plasma Mass Spectrometry to quantify sodium in selected skin samples.Results: Human dermis has a preponderance (>90%) of bound sodium that co-localizes with the glycosaminoglycan (GAG) scaffold. Bound and free sodium have similar anatomical locations. T2D associates with a severely reduced dermal bound sodium capacity. Conclusion:We provide the first evidence for high levels of bound sodium within human dermis, co-locating to the GAG scaffold, consistent with a dermal 'third space repository' for sodium. T2D associates with diminished dermal electrostatic binding capacity for sodium.