Obesity is a chronic, complex and multi-factorial condition with an increasing prevalence worldwide. Irregular eating schedules might be a contributing factor to these numbers through the dysregulation of the circadian system. Time-restricted eating (TRE), an approach that limits eating windows, has been studied as a strategy to treat obesity, aligning eating occasions with metabolic circadian rhythms. This review aims to provide an overview of the impact of TRE protocols on metabolic, inflammatory, oxidative stress, and circadian rhythm biomarkers in people with overweight or obesity. Most studies report significant weight loss following TRE protocols. While glucose levels decreased in nearly all TRE interventions, only a few studies demonstrated statistically significant differences when compared to the control groups. The findings for CRP and TNF-α were inconsistent, with limited significant differences. Changes in lipid profile changes were variable and generally did not reach statistical significance. Both 4-hour and 6-hour TRE interventions significantly reduced 8-isoprostane levels. Additionally, TRE significantly altered clock gene expression, as well as that of genes associated with metabolic regulation in subcutaneous adipose tissue. While the evidence is still inconsistent, limiting eating to a consistent daily window of 8 to 12 hours can improve insulin sensitivity, reduce blood glucose, cholesterol and triglyceride levels and promote weight loss. These effects are likely attributable to both direct metabolic impacts and indirect benefits from weight loss and improved dietary habits. However, data on circadian, inflammatory, and specific metabolic biomarkers remain scarce and occasionally contradictory, highlighting the need for further research on these interventions.

Emerging evidence suggests that low-grade systemic inflammation plays a key role in altering brain activity, behaviour and affect. Modulation of the gut microbiota using prebiotic fibre offers a potential therapeutic tool to regulate inflammation, mediated via the production of short-chain fatty acids (SCFA). However, the impact of prebiotic consumption on affective symptoms and the possible contribution from inflammation, gut symptoms and the gut microbiome are currently underexamined. In this 12-week study, the effects of a diverse prebiotic blend on inflammation, gut microbiota profiles and affective symptoms in a population with metabolic syndrome (MetS) were examined. Sixty males and females with MetS meeting the criteria for MetS were randomised into a treatment group (n 40), receiving 10 g per day of a diverse prebiotic blend and healthy eating advice, and a control group (n 20), receiving healthy eating advice only. Our results showed a significant reduction in high sensitivity C-reactive protein (hs-CRP) in the treatment (–0·58 [–9·96 to–2·63]) compared with control (0·37 [–3·64 to–3·32]), alongside significant improvements in self-reported affective scores in the treatment compared with the control group. While there were no differences in relative abundance between groups at week 12, there was a significant increase from baseline to week 12 in fecal Bifidobacterium and Parabacteroides in the treatment group, both of which are recognised as SCFA producers. Multivariate regression analyses further revealed an association between gastrointestinal symptoms and hs-CRP with affective scores. Together, this study provides preliminary support for a diverse prebiotic blend for mood, stress and anxiety.

It is estimated that one-quarter of the world’s population has Metabolic Syndrome (MS)(1), a key driver of growth in healthcare expenditure. Traditional approaches to treating MS through the application of standard dietary recommendations and caloric restriction have had limited success. More recent evidence suggests that novel, anti-inflammatory approaches such as replacing refined carbohydrates and ultra-processed food with unprocessed or minimally processed, lower carbohydrate foods and adapting meal timing and frequency may be more effective(2). The aim of the study was twofold: 1) To determine the effectiveness of anti-inflammatory dietary strategies for long-term weight loss and improvement in metabolic health and 2) To examine the relationships between eating behaviours and long-term weight loss. Twelve-month audit data from a UK based 12-week lifestyle program that focuses the principles of consuming an anti-inflammatory diet was analysed using repeated-measures ANOVA to examine the effects of the program on changes in weight and waist circumference. A quantitative, survey-based research design was used to retrospectively identify relationships between eating behaviours and both anti-inflammatory and pro-inflammatory dietary patterns. Multivariate regression using stepwise method was used to examine differences in weight change based on eating patterns and behaviours. Six hundred and forty-two (N = 642) participants (age = 50.4 ± 12.5 years, female 63.6%, weight = 96.1 kg ± 22.1, BMI 35.2 kg/m2 ± 7.5) demonstrated a weight loss average of 4.49 kg ± 3.78 post-lifestyle program (12 weeks). Survey respondents (N = 64) reported a maximum long term weight loss of 13.9 kg ± 11.9. Weight loss and percentage weight loss after the program was significantly predicted by daily consumption of sweet drinks and grain-based foods. The model predicted one unit increase in daily serving consumption of these foods resulted in less weight lost [2.3 kg (4.5%)]. Seventy one percent of survey respondents had maintained most or all their weight loss for more than 6 months. The model predicted change in consumption of grain-based foods, TFEQ-emotional eating score, consumption of savoury ultra-processed foods, and following an alternative dietary approach after the program were statistically significant in predicting weight loss maintenance (R2 = 0.803, F(4, 20) = 20.376, p < 0.001). The preliminary findings suggest that anti-inflammatory dietary approaches are effective and sustainable for weight loss. Eating behaviour may both support and hinder long term changes in eating patterns and whilst there are significant relationships between eating behaviour and eating patterns, the extent to which dietary patterns drive eating behaviour remains unclear.

Cardiometabolic diseases are highly prevalent in Aotearoa New Zealand(1). Dietary intake is a modifiable risk factor for such diseases and certain dietary patterns, specifically the Mediterranean diet (MedDiet), are associated with improved metabolic health(2). This study aims to test whether an intervention of a Mediterranean dietary pattern incorporating high quality New Zealand foods (NZMedDiet pattern) using behaviour change science can improve the metabolic health of participants and their household/whānau. This is a multi-centre, three-stage trial, with two randomised controlled trials (RCTs), both parallel groups, superiority trials, and a longitudinal cohort study. The first RCT (RCT1) is a comparison of the NZMedDiet pattern implemented using behaviour science compared to usual diet for 12 weeks, and the second (RCT2) is a behaviour-change intervention compared to no intervention for 12 weeks, administered after participants have been exposed to the intervention in RCT1. The third stage is a longitudinal cohort study where all participants are followed for up to a year. The primary outcome measure for each stage is the metabolic syndrome severity score (MetSSS). Two hundred index participants and their household/whānau have been recruited and randomised into the trial. Participants are from four centres, two of which are University research units (University of Auckland (n = 57) and University of Otago, Christchurch (n = 60)), one a community-based traditional meeting place (Tu¯ Kotahi Māori Asthma and Research Trust at Ko¯kiri Marae in Lower Hutt, Wellington (n = 19)), and the other based at a hospital-based research unit (the Centre for Endocrine Diabetes and Obesity Research (CEDOR) in Wellington (n = 64). The trial will test whether the NZMedDiet pattern and behaviour change support improves the cardiometabolic health of people in New Zealand.

Carotenoids are generally associated with health-beneficial effects; however, their intake patterns related to the metabolic syndrome (MetS) and its components remain controversial. This cross-sectional study investigated associations between dietary intakes of individual carotenoids, fruits and vegetables, and the MetS and its components. Dietary intakes of 1346 participants of the Observation des Risques et de la Santé Cardio-Vasculaire au Luxembourg (ORISCAV-LUX-2) study were investigated by a 174-item FFQ, and carotenoid intake was determined by linking findings using mainly the USDA food databases. Components of MetS and complementary variables, including anthropometric (BMI, waist circumferences and waist:hip ratio) and biological parameters (TAG, HDL-cholesterol, fasting blood glucose and blood pressure), were measured. Logistic (for MetS) and linear multivariable regression models (including assessing MetS as scores) adjusted for various confounders were created. α-and β-Carotene, as well as lutein + zeaxanthin, were inversely associated with MetS (also when it was measured on a continuous scale), reducing the odds for MetS by up to 48 %. However, lycopene, phytoene and phytofluene were rather positively associated with MetS scores and its components, though these adverse effects disappeared, at least for lycopene, when controlling for intakes of tomato-based convenience foods, in line with indicating a rather unhealthy/westernised diet. All these associations remained significant when including fruits and vegetables as confounders, suggesting that carotenoids were related to MetS independently from effects within fruits and vegetables. Thus, a high intake of carotenoids was bidirectionally associated with MetS, its severity, risk and its components, depending on the type of carotenoid. Future investigations are warranted to explore the inverse role that tomato-based carotenoids appear to suggest in relation to the MetS.

Individuals with mood disorders are predisposed to metabolic dysfunction, while those with metabolic dysregulation such as diabetes and obesity experience more severe depressive symptoms. Both metabolic dysfunction and mood disorders are independently associated with cognitive deficits. Therefore, given their close association, this study aimed to explore the association between metabolic dysfunction in individuals with mood disorders in relation to cognitive outcomes. A comprehensive search comprised of these three domains was carried out; a random-effects meta-analysis pooling mean cognitive outcomes was conducted (PROSPERO ID: CRD42022295765). Sixty-three studies were included in this review; 26 were synthesized in a quantitative meta-analysis. Comorbid metabolic dysregulation was associated with significantly lower global cognition among individuals with mood disorders. These trends were significant within each mood disorder subgroup, including major depressive disorder, bipolar disorder, and self-report depression/depressive symptoms. Type 2 diabetes was associated with the lowest cognitive performance in individuals with mood disorders, followed by peripheral insulin resistance, body mass index ⩾25 kg/m2, and metabolic syndrome. Significant reduction in scores was also observed among individual cognitive domains (in descending order) of working memory, attention, executive function, processing speed, verbal memory, and visual memory. These findings demonstrate the detrimental effects of comorbid metabolic dysfunction in individuals with mood disorders. Further research is required to understand the underlying mechanisms connecting mood disorders, metabolism, and cognition.

Obesity is an important characteristic manifestation of metabolic syndrome (MetS), and body roundness index (BRI) is one of the anthropometric indicators associated with obesity. However, studies on the relationship between BRI and MetS risk are limited. We aimed to explore the relationship between baseline BRI and MetS in the USA population. Our study used data from the National Health and Nutrition Examination Survey from 1999 to 2018, ultimately enrolling and analysing 47 303 participants. Data-driven tertiles were used to categorise BRI levels, and multivariate logistic regression models were fitted to investigate the association of BRI with MetS in adults. In addition, receiver operating characteristic curve analysis was used to assess the ability of BRI to predict MetS. The distribution of BRI was different across ethnic groups with a gradual decrease in the proportion of non-Hispanic Whites and other races. In addition, BRI was significantly associated with traditional cardiovascular risk factors. Univariate regression analysis indicated BRI to be a moderate risk factor for MetS, and multivariate logistic regression analysis found that BRI remained an independent risk factor for MetS. After adjusting for confounding variables, a non-linear relationship was found between BRI levels and the prevalence of MetS. More importantly, BRI predicted MetS with the largest AUC among anthropometric measures. In summary, elevated baseline BRI levels are independently associated with the development of MetS, and baseline BRI may assist in identifying patients at risk for MetS, leading to early and optimal treatment to improve their outcomes.

The main cause of mortality in great apes in zoological settings is cardiovascular disease (CVD), affecting all four taxa: chimpanzee (Pan troglodytes), bonobo (Pan paniscus), gorilla (Gorilla spp.) and orangutan (Pongo spp.). Myocardial fibrosis, the most typical histological characterisation of CVD in great apes, is non-specific, making it challenging to understand the aetiopathogenesis. A multifactorial origin of disease is assumed whereby many potential causative factors are directly or indirectly related to the diet, which in wild-living great apes mainly consists of high-fibre, low-carbohydrate and very low-sodium components. Diets of great apes housed in zoological settings are often different compared with the situation in the wild. Moreover, low circulating vitamin D levels have recently been recognised in great apes housed in more northern regions. Evaluation of current supplementation guidelines shows that, despite implementation of different dietary strategies, animals stay vitamin D insufficient. Therefore, recent hypotheses designate vitamin D deficiency as a potential underlying factor in the pathogenesis of myocardial fibrosis. The aim of this literature review is to: (i) examine important differences in nutritional factors between zoological and wild great ape populations; (ii) explain the potential detrimental effects of the highlighted dietary discrepancies on cardiovascular function in great apes; and (iii) elucidate specific nutrition-related pathophysiological mechanisms that may underlie the development of myocardial fibrosis. This information may contribute to understanding the aetiopathogenesis of myocardial fibrosis in great apes and pave the way for future clinical studies and a more preventive approach to great ape CVD management.

Malnutrition is a key factor in metabolic syndrome (MS) and sarcopenia, assessing the nutritional status of these patients is a pressing issue. The purpose of this study was to clarify sarcopenia and sarcopenic obesity in patients with MS based on nutritional status. This was a case–control study between MS/non-MS. Body composition was measured by dual-energy X-ray absorptiometry. Muscle function was assessed by handgrip strength, five times sit-to-stand test, gait speed test and short physical performance battery (SPPB). The Mini Nutritional Assessment (MNA) was performed to assess the nutritional status in the participants in this study. Overall, a total of 56 % and 13 % of participants suffered from possible sarcopenia and sarcopenia, respectively. There was a higher rate of possible sarcopenic obesity in the MS group than in the non-MS group (48·9 % v. 24·7 %, P < 0·01), and all the sarcopenia participants in the MS group had sarcopenic obesity. MNA score was significantly associated with sarcopenia status (P < 0·01). The MNA combined with body fat score showed better acceptable discrimination for detecting sarcopenic obesity and sarcopenia in MS (AUC = 0·70, 95 % CI 0·53, 0·86). In summary, there was a higher prevalence of possible sarcopenic obesity in MS, and all the MS patients with sarcopenia had sarcopenic obesity in the present study. We suggest that the MNA should be combined with body fat percentage to assess the nutritional status of MS participants, and it also serves as a good indicator for sarcopenia and sarcopenic obesity in MS.

Curcumin is a phytocompound found in the root of turmeric, a common herbal ingredient in many Asian cuisines. The compound contains anti-inflammatory activity, which is mediated through an upregulation of adiponectin and reduction of leptin. Results of randomised controlled trials (RCT) have shown that the effects of curcumin on adipokines are conflicting. Therefore, the current systematic review and meta-analysis of RCT were conducted with the aim of elucidating the role of curcumin supplementation on serum adiponectin and leptin. The search included PubMed, Embase, Cochrane Library, Scopus, Web of Science and Google Scholar from inception to August 2023. For net changes in adipokines, standardised mean differences (SMD) were calculated using random effects models. Thirteen RCT with fourteen treatment arms were eligible for inclusion in this meta-analysis. Curcumin supplementation was effective in increasing serum adiponectin (SMD = 0·86, 95 % CI (0·33, 1·39), P < 0·001; I2 = 93·1 %, P < 0·001) and reducing serum leptin (SMD = −1·42, 95 % CI (−2·29, −0·54), P < 0·001; I2 = 94·7 %, P < 0·001). In conclusion, curcumin supplementation significantly increased circulating adiponectin and decreased leptin levels in adults.

Stress and diabetes coexist in a vicious cycle. Different types of stress lead to diabetes, while diabetes itself is a major life stressor. This was the focus of the Chicago Biomedical Consortium’s 19th annual symposium, “Stress and Human Health: Diabetes,” in November 2022. There, researchers primarily from the Chicago area met to explore how different sources of stress – from the cells to the community – impact diabetes outcomes. Presenters discussed the consequences of stress arising from mutant proteins, obesity, sleep disturbances, environmental pollutants, COVID-19, and racial and socioeconomic disparities. This symposium showcased the latest diabetes research and highlighted promising new treatment approaches for mitigating stress in diabetes.

Gestational obesity has major negative impacts on both mothers and their offspring. More than two-thirds of women of reproductive age in the United States are overweight and/or obese. We previously reported that the source of protein in the maternal diet influences the phenotype of offspring born to normal-weight dams. However, whether it has the same effect in obese mothers was unclear. The casein- and soya protein-based diets were fed to obese pregnant Wistar rats and compared for their effects on characteristics of the metabolic syndrome in male offspring. Dams randomized to either a casein (CD) or soya protein (SD) diet (n 12). Pups were weaned to either a CD or SD for 16 weeks. Offspring of SD dams had higher birthweight (P < 0⋅01). Glucose metabolism was not altered at birth but fasting blood glucose (FBG) (P < 0⋅02), insulin (P < 0⋅0002), insulin/glucose ratio (P < 0⋅03), and HOMA-IR index (P < 0⋅0002) were higher in offspring of SD dams at week 17. The pulse rate was higher in dams (P < 0⋅03). Food intake and body weight of offspring were affected by interactive effects of time and dams’ diet (P < 0⋅05). Food intake was not influenced by maternal diet, but it was higher in pups weaned to SD dams (P < 0⋅03) The results of this study indicate that although the source of protein in the maternal diet is still an influencing factor in the outcome of the pregnancy in obese mothers, gestational obesity may mask this effect possibly by imposing general detrimental effects on measured parameters regardless of the source of protein in maternal diet.