University life is a critical period for establishing healthy eating habits and attitudes. However, university students are at risk of developing poor eating habits due to various factors, including economic conditions, academic stress and lack of information about nutritional concepts. Poor diet quality leads to malnutrition or overnutrition, increasing the risk of preventable diseases. Food environments on university campuses also play a significant role in shaping the dietary habits of students, with the availability of and accessibility to healthy food options being important factors influencing food choices and overall diet quality. Disordered eating habits and body dissatisfaction are prevalent among university students and can lead to eating disorders. Income and living arrangements also influence dietary habits, with low household income and living alone being associated with unhealthy eating habits. This study is a narrative review that aimed to address nutritional issues and eating behaviours, specifically among university students. We investigated the eating behaviours of university students, including their dietary patterns, food choices and food environments. The objective of this review was to provide insights into the nutritional issues and eating behaviours of university students, with the aim of identifying target areas for intervention to improve the overall health and wellbeing among college students. University food environments need to be restructured to promote healthy eating, including the availability, accessibility, affordability and labelling of healthy foods, and policies to limit the availability of unhealthy foods and drinks on campus.

The increasing rates of obesity are contributing to a decrease in life expectancy in the USA. Although innovative obesity therapies are being developed, they alone will not suffice to combat the widespread obesity epidemic. Patients with overweight and obesity face incredible headwinds in an increasingly obesogenic food environment derived from previous and current food, agricultural, and governmental policies. Regional policies contribute to the development of food swamps, which exert an even more substantial influence on weight gain than food deserts. Grocery store layouts and marketing practices perpetuate unhealthy food purchases among low-income individuals. Furthermore, national agricultural policies have contributed to increased portion sizes and a supply of ultra-processed foods. To effectively treat and advocate for patients, general internists must understand how these policies drive the obesity epidemic. In this review, we dissect the marketing practices and regional and national food policies that contribute to the obesogenic food environment. We also highlight policies that provide evidence for improving the food environment and reversing the obesity epidemic.

The hypothalamus (HT) plays a crucial role in regulating eating behaviors. Disruptions in its function have been linked to the development of weight-related disorders. Nevertheless, its characterization remains a challenge.

We assessed the structural alterations of individual HT nuclei related to eating behaviors in patients with weight-related disorders, and their association with body mass index (BMI) and severity of eating disorders.

Forty-four young females with normal weight (HC, n = 21), restrictive anorexia nervosa (AN, n = 13), and living with obesity (OB, n = 10) were explored in vivo using 7-T high-resolution (0.6 mm isotropic voxel) T1 quantitative magnetic resonance imaging (MRI). Volumes and quantitative T1 values of individual HT nuclei were compared after whole-brain normalization using nonparametric tests (corrected for multiple comparisons for groups and regions). We investigated the parameters associated with BMI and eating disorders, such as MRI parameters of HT nuclei, ghrelin and leptin levels, depression, and anxiety using multivariate nonlinear partial least square (NIPALS).

Both AN and OB showed higher volumes of HT relative to HC (Zscores: 0.78 ± 1.06; 1.43 ± 1.51). AN showed significantly higher volumes and T1 values of the right paraventricular nucleus (PaVN) (volume Zscore: 1.82 ± 1.45; T1 Zscore: 3.76 ± 4.67), and higher T1 values of the left PaVN (Zscore: 2.25 ± 2.37) and right periventricular nuclei (Zscore: 3.73 ± 4.81). NIPALS models showed that lower BMI in AN was associated with structural alterations of the bilateral PaVN, right anterior commissure, and left fornix (FX). Higher BMI in OB was associated with structural alterations within the right PaVN, bilateral FX, left posterior hypothalamic nucleus, right lateral HT, and right anterior hypothalamic area. Finally, the severity of eating disorders was associated with larger structural alterations within the bilateral PaVN, bilateral arcuate hypothalamic nuclei, right bed nucleus of stria terminalis, left medial preoptic nucleus, and right tubero-mammillary hypothalamic nucleus.

Weight-related disorders are associated with significant micro and macrostructural alterations in HT nuclei involved in eating behaviors.

In everyday life, dietary decisions are made in response to real foods, such as at the grocery store or cafe. In stark contrast, decision-making studies in the laboratory typically measure responses to food stimuli presented as two-dimensional pictures or computer images, with the assumption that artificial displays are adequate substitutes for their real-world counterparts. Yet accumulating evidence challenges this view, including studies showing that willingness-to-pay (WTP) is higher for foods displayed as real objects versus images -a phenomenon known as the "real object advantage" in valuation. Here, we examined whether the "real object advantage" is modulated by accessibility to the stimuli, subjective food preference, or interactions between these factors. Participants placed monetary bids on snack foods displayed as real objects or computer images. Critically, on half of the trials, a transparent barrier was positioned between the participant and the stimulus. Linear mixed-effects modeling analysis revealed that, overall, WTP was ∼7 % higher for foods displayed as real objects versus images; however, this effect emerged only for foods of moderate (but not strong) preference strength. WTP was also higher when the stimuli appeared unoccluded versus behind the barrier, but this was equally so for real objects and images, suggesting that the barrier's effect on valuation was not related to stimulus actability. Our findings suggest that while eliminating perceived barriers to a good can bolster valuation regardless of display format, presenting real foods may nevertheless increase valuation and encourage healthy dietary choices.

Higher ultra-processed food and drink (UPFD) consumption has been linked with increased risk of non-communicable diseases. Low-grade systemic inflammation may partly underlie this relationship, yet limited research on UPFDs exists in this context. We examined UPFD associations with inflammatory biomarkers and explored whether relationships are mediated by adiposity.

This was a cross-sectional study of 1,986 middle- to older-aged men and women. Using the NOVA classification, UPFD weight ratios were calculated for each participant. Correlation and multivariate-adjusted linear regression analyses were used to test UPFD intake associations with a wide range of inflammatory biomarkers. Mediation analyses explored whether relationships were independent or mediated by adiposity, defined by body mass index (BMI) or waist-height ratio (WHtR).

Significant direct effects between UPFD consumption and higher levels of interleukin 6, tumour necrosis factor-alpha, white blood cell counts and constituent neutrophils, basophils, and the neutrophil-to-lymphocyte ratio, were observed in models which controlled for a range of potential confounders, and which additionally adjusted for BMI or WHtR. Higher levels of adiposity were found to mediate relationships between UPFD intake and biomarkers, with the percentage of total effect mediated ranging from 12.7 to 70.1% for models including BMI, and 13.5 to 64.5% for models including WHtR.

Consumption of UPFDs is associated with a less optimal inflammatory biomarker profile and the total effect of UPFD intake on biomarker concentrations is likely due both to higher levels of adiposity related to UPFD consumption and the pro-inflammatory potential of UPFD products.

Calorie-rich foods, particularly those that are high in fat and sugar, evoke pleasure in both humans and animals1. However, prolonged consumption of such foods may reduce their hedonic value, potentially contributing to obesity2-4. Here we investigated this phenomenon in mice on a chronic high-fat diet (HFD). Although these mice preferred high-fat food over regular chow in their home cages, they showed reduced interest in calorie-rich foods in a no-effort setting. This paradoxical decrease in hedonic feeding has been reported previously3-7, but its neurobiological basis remains unclear. We found that in mice on regular diet, neurons in the lateral nucleus accumbens (NAcLat) projecting to the ventral tegmental area (VTA) encoded hedonic feeding behaviours. In HFD mice, this behaviour was reduced and uncoupled from neural activity. Optogenetic stimulation of the NAcLat→VTA pathway increased hedonic feeding in mice on regular diet but not in HFD mice, though this behaviour was restored when HFD mice returned to a regular diet. HFD mice exhibited reduced neurotensin expression and release in the NAcLat→VTA pathway. Furthermore, neurotensin knockout in the NAcLat and neurotensin receptor blockade in the VTA each abolished optogenetically induced hedonic feeding behaviour. Enhancing neurotensin signalling via overexpression normalized aspects of diet-induced obesity, including weight gain and hedonic feeding. Together, our findings identify a neural circuit mechanism that links the devaluation of hedonic foods with obesity.

Maladaptive feeding comprises unhealthy eating patterns that jeopardize survival, including over- and underconsumption. These behaviors are often coordinated by endogenous opioid receptors (EORs). Here, we explore the involvement of EORs in obesity and anorexia nervosa (AN), two disorders associated with dysregulated feeding behavior and relevant animal models. While seemingly opposing metabo-psychiatric states, our goal is to highlight common circuit and synaptic mechanisms underlying obesity and AN with a focus on EOR functionality. We examine the neural substrates underlying maladaptive feeding and comorbid conditions including pain, suggesting a role for EOR-driven plasticity in the pathogenesis of both obesity and AN.

Human regulatory systems largely evolved under conditions of food and information scarcity but are now being forced to deal with abundance. The impact of abundance and the inability of human regulatory systems to adapt to it have fed a surge in dual health challenges: (1) a rise in obesity related to food abundance and (2) a rise in stress and anxiety related to information abundance. No single framework has been developed to describe why and how the transition from scarcity to abundance has been so challenging. Here, we provide a speculative model based on predictive processing. We suggest that whereas scarcity (above destructive lower bounds like famine or information voids) preserves the fidelity of the relationship between prediction errors and predictions, abundance distorts this relationship. Furthermore, prediction error minimization is enhanced under scarcity (as the number of competing states in the niche is restricted), whereas the opposite is true under abundance. We also discuss how abundance warps the fundamental drive for seeking novelty by fueling the brain's exploration (as opposed to exploitation) mode. Ameliorative strategies for regulating food and information abundance may largely depend on simulating scarcity, that environmental condition to which human regulatory systems have adapted over millennia.

In modern society, excessive nutrient intake from food is a major factor contributing to the development of a series of metabolic disorders and cardiovascular diseases. Further investigation of the mechanisms underlying nutrient absorption in the intestine will help to better understand and develop preventive or therapeutic strategies. In this study, using receptor-interacting protein kinase 1 (Ripk1) intestine-specific heterozygous knockout mice (Ripk1 IEC+/-) and high-fat diet (HFD)-feeding mouse model, we report that HFD-induced shift in the transcriptional profile of the ileum toward that of the jejunum, characterized by increased expression of jejunal feature genes in the ileum, are attenuated in Ripk1 IEC+/- female mice, but not in males. Accordingly, HFD-induced metabolic disorders, including obesity, impaired glucose tolerance, insulin resistance, and dyslipidemia, are significantly ameliorated in the Ripk1 IEC+/- female mice. These findings demonstrate a new, sex-specific intestinal regulatory mechanism and highlight the critical role of intestinal RIPK1 in regulating HFD-induced metabolic disorders in females.

Over the past several decades, the overweight and obesity epidemic in the USA has resulted in a significant health and economic burden. Understanding current trends and future trajectories at both national and state levels is crucial for assessing the success of existing interventions and informing future health policy changes. We estimated the prevalence of overweight and obesity from 1990 to 2021 with forecasts to 2050 for children and adolescents (aged 5-24 years) and adults (aged ≥25 years) at the national level. Additionally, we derived state-specific estimates and projections for older adolescents (aged 15-24 years) and adults for all 50 states and Washington, DC.

In this analysis, self-reported and measured anthropometric data were extracted from 134 unique sources, which included all major national surveillance survey data. Adjustments were made to correct for self-reporting bias. For individuals older than 18 years, overweight was defined as having a BMI of 25 kg/m2 to less than 30 kg/m2 and obesity was defined as a BMI of 30 kg/m2 or higher, and for individuals younger than 18 years definitions were based on International Obesity Task Force criteria. Historical trends of overweight and obesity prevalence from 1990 to 2021 were estimated using spatiotemporal Gaussian process regression models. A generalised ensemble modelling approach was then used to derive projected estimates up to 2050, assuming continuation of past trends and patterns. All estimates were calculated by age and sex at the national level, with estimates for older adolescents (aged 15-24 years) and adults aged (≥25 years) also calculated for 50 states and Washington, DC. 95% uncertainty intervals (UIs) were derived from the 2·5th and 97·5th percentiles of the posterior distributions of the respective estimates.

In 2021, an estimated 15·1 million (95% UI 13·5-16·8) children and young adolescents (aged 5-14 years), 21·4 million (20·2-22·6) older adolescents (aged 15-24 years), and 172 million (169-174) adults (aged ≥25 years) had overweight or obesity in the USA. Texas had the highest age-standardised prevalence of overweight or obesity for male adolescents (aged 15-24 years), at 52·4% (47·4-57·6), whereas Mississippi had the highest for female adolescents (aged 15-24 years), at 63·0% (57·0-68·5). Among adults, the prevalence of overweight or obesity was highest in North Dakota for males, estimated at 80·6% (78·5-82·6), and in Mississippi for females at 79·9% (77·8-81·8). The prevalence of obesity has outpaced the increase in overweight over time, especially among adolescents. Between 1990 and 2021, the percentage change in the age-standardised prevalence of obesity increased by 158·4% (123·9-197·4) among male adolescents and 185·9% (139·4-237·1) among female adolescents (15-24 years). For adults, the percentage change in prevalence of obesity was 123·6% (112·4-136·4) in males and 99·9% (88·8-111·1) in females. Forecast results suggest that if past trends and patterns continue, an additional 3·33 million children and young adolescents (aged 5-14 years), 3·41 million older adolescents (aged 15-24 years), and 41·4 million adults (aged ≥25 years) will have overweight or obesity by 2050. By 2050, the total number of children and adolescents with overweight and obesity will reach 43·1 million (37·2-47·4) and the total number of adults with overweight and obesity will reach 213 million (202-221). In 2050, in most states, a projected one in three adolescents (aged 15-24 years) and two in three adults (≥25 years) will have obesity. Although southern states, such as Oklahoma, Mississippi, Alabama, Arkansas, West Virginia, and Kentucky, are forecast to continue to have a high prevalence of obesity, the highest percentage changes from 2021 are projected in states such as Utah for adolescents and Colorado for adults.

Existing policies have failed to address overweight and obesity. Without major reform, the forecasted trends will be devastating at the individual and population level, and the associated disease burden and economic costs will continue to escalate. Stronger governance is needed to support and implement a multifaceted whole-system approach to disrupt the structural drivers of overweight and obesity at both national and local levels. Although clinical innovations should be leveraged to treat and manage existing obesity equitably, population-level prevention remains central to any intervention strategies, particularly for children and adolescents.

Bill & Melinda Gates Foundation.

The human gut is a complex ecosystem that supports billions of living species, including bacteria, viruses, archaea, phages, fungi, and unicellular eukaryotes. Bacteria give genes and enzymes for microbial and host-produced compounds, establishing a symbiotic link between the external environment and the host at both the gut and systemic levels. The gut microbiome, which is primarily made up of commensal bacteria, is critical for maintaining the healthy host's immune system, aiding digestion, synthesizing essential nutrients, and protecting against pathogenic bacteria, as well as influencing endocrine, neural, humoral, and immunological functions and metabolic pathways. Qualitative, quantitative, and/or topographic shifts can alter the gut microbiome, resulting in dysbiosis and microbial dysfunction, which can contribute to a variety of noncommunicable illnesses, including hypertension, cardiovascular disease, obesity, diabetes, inflammatory bowel disease, cancer, and irritable bowel syndrome. While most evidence to date is observational and does not establish direct causation, ongoing clinical trials and advanced genomic techniques are steadily enhancing our understanding of these intricate interactions. This review will explore key aspects of the relationship between gut microbiota, eubiosis, and dysbiosis in human health and disease, highlighting emerging strategies for microbiome engineering as potential therapeutic approaches for various conditions.

Childhood obesity is a growing global public health problem. Studies suggest that environmental cues contribute to developing and maintaining obesity. We aimed to evaluate pupillary changes to auditory food words vs. nonfood words and to conduct a dynamic temporal analysis of pupil size changes in adolescents with obesity without binge eating disorder by comparing healthy-weight adolescents. In this study, a total of 63 adolescents aged 12-18 years (n = 32, obesity group (OG); n = 31, control group (CG)) were included. In an auditory paradigm, participants were presented with a series of high and low-calorie food and nonfood words. A binocular remote eye-tracking device was used to measure pupil diameter. Generalized additive mixed models (GAMMs) were used for dynamic temporal analysis of pupillometry data. The results of GAMM analysis indicated that CG had larger pupil dilation than the OG while listening to auditory food words. CG had larger pupil dilation in food words than in nonfood words. However, the OG had a similar pupillary response in food and nonfood words. Pupil dilation response to higher-calorie foods was extended over the later stages of the time period (after 2000 ms) in the OG. In summary, our findings indicated that individuals with obesity had lower pupil dilation to auditory food words compared to normal-weight peers. Adolescents with obesity had prolonged pupillary dilation in higher calories of food words. The individual psychological factors affecting the dynamic changes of pupil responses to food cues in adolescents with obesity should be examined in further studies.

Diets that are high in fat cause over-eating and weight gain in multiple species of animals, suggesting that high dietary fat is sufficient to cause obesity. However, high-fat diets are typically provided freely to animals in obesity experiments, so it remains unclear if high-fat diets would still cause obesity if they required more effort to obtain. We hypothesized that unrestricted and easy access is necessary for high-fat diet induced over-eating, and the corollary that requiring mice to perform small amounts of work to obtain high-fat diet would reduce high-fat diet intake and associated weight gain. To test this hypothesis, we developed a novel home-cage based feeding device that either provided high-fat diet freely, or after mice poked their noses into a port one time - a simple action that is easy for them to do. We tested the effect of this intervention for six weeks, with mice receiving all daily calories from high-fat diet, modifying only how they accessed it. Requiring mice to nose-poke to access high-fat diet reduced intake and nearly completely prevented the development of obesity. In follow up experiments, we observed a similar phenomenon in mice responding for low-fat grain-based pellets that do not induce obesity, suggesting a general mechanism whereby animals engage with and consume more food when it is freely available vs. when it requires a simple action to obtain. We conclude that unrestricted access to food promotes overeating, and that a simple action such as a nose-poke can reduce over-eating and weight gain in mice. This may have implications for why over-eating and obesity are common in modern food environments, which are often characterized by easy access to low-cost unhealthy foods.

South Africa is experiencing a persistent growth in non-communicable diseases. Diabetes is among the top ten causes of mortality, especially among women, which is partly driven by high levels of added sugar consumption and obesity. To reduce obesity rates and the incidence of diabetes, South Africa introduced a tax on sugar sweetened beverages (also known as the Health Promotion Levy (HPL)) in 2018. The tax is applicable to sugar-sweetened beverages but excludes 100% fruit juice. The government is currently considering extending the tax to include fruit juices. This study models the potential health and economic impact of taxing fruit juices at 20% of the retail price of one liter.

To analyze the distributional impact of the tax, this study uses extended cost-effectiveness analysis methodology. Data on price elasticities, healthcare cost, income, fruit juice consumption were sourced from the literature and representative national surveys. The potential impact of the tax on diabetes incidence, prevalence, mortality, and financial benefits were estimated for each income group (lowest, quintile 1 to highest, quintile 5).

We estimate that a 20% tax on fruit juice would avert 156,640 incident cases of type 2 diabetes mellitus over 20 years, with most disease averted occurring among the first- and fifth-income groups. Averted deaths from diabetes would average 2,000 deaths per quintile (for quintiles 1 to 4) and about 2,800 in quintile 5. The improved health resulting from averted incidence and deaths will reduce overall healthcare expenditure by R7.5 billion over 20 years, of which R2.3 billion will occur in the fifth quintile. The South African government will also save about R300 million in subsidizing diabetes-related healthcare cost as a result of prevention; and would raise R8.6 billion in tax revenues per annum. Out-of-pocket expenditure savings will be R303 million and a financial risk protection (money-metric value of insurance) of R4.6 billion over the 20-year period.

We conclude that an HPL that significantly raises the retail price of fruit juices would reduce consumption and diabetes-related morbidity and mortality. The tax will also provide significant financial benefits in the form of reduced healthcare costs for both government and households as well as providing financial risk protection to individuals. Health taxes are win-win policies that improve population health and generate revenue for governments to fund public health services delivery and thus improve overall health financing activities of the government. Therefore, population level disease prevention measures such as health taxes are important for achieving universal health coverage.

Studying the dietary antioxidant quality (DAQ) score as a modifiable factor to lessen the negative effects of obesity on health is vital due to the rising global trend of obesity. Therefore, this study aimed to determine how adult obesity and meal-based DAQ scores correlate.

A cross-sectional study including 850 men and women in Tehran was conducted. Three 24-hour dietary recalls were used to evaluate dietary consumption. Based on the design of DAQs, the meal-based DAQ score was evaluated. Higher scores indicate better DAQ. The overall DAQ score varied from 0 to 5. To investigate the relationship between DAQs and obesity in each meal, logistic regression analysis was utilized.

There was no correlation between a higher breakfast DAQ score and being overweight or obese (for overweight: OR = 0.69; 95% CI: 0.38-1.24/for obesity: OR = 0.65; CI 95%: 0.31-1.37). In the basic model, a higher lunch DAQ score was inversely related to probabilities of being overweight (OR: 0.62; 95% CI: 0.39-0.99) Such a connection remained significant after relevant confounders were considered (OR: 0.48; 95% CI: 0.27-0.84). In both the raw and fully adjusted models, there was no discernible correlation between the meal DAQ score and overweight or obesity.

We discovered that a higher DAQ score for lunch was substantially associated with a lower risk of being overweight but not obese. To verify our findings, additional prospective research in various populations is required.

Chronic pain and obesity frequently occur together. An ideal therapy would alleviate pain without weight gain, and most optimally, could promote weight loss. The neuropeptide neurotensin (Nts) has been separately implicated in reducing weight and pain but could it be a common actionable target for both pain and obesity? Here we review the current knowledge of Nts signaling via its receptors in modulating body weight and pain processing. Evaluating the mechanism by which Nts impacts ingestive behavior, body weight, and analgesia has potential to identify common physiologic mechanisms underlying weight and pain comorbidities, and whether Nts may be common actionable targets for both.

Studies have consistently demonstrated associations between ultra-processed food and drink (UPFD) consumption and non-communicable diseases. However, there is a lack of data investigating relationships between UPFD intake and intermediate cardiometabolic disease markers. In this study we explored UPFD associations with lipoprotein subclasses.

This was a cross-sectional study of 1986 middle-to older-aged men and women randomly selected from a large primary care centre. The percentage contribution of UPFDs to total energy intake was calculated for each participant using the NOVA classification. Lipoprotein particle subclass concentrations and size were determined using nuclear magnetic resonance spectroscopy. Correlation and multivariate-adjusted linear regression analyses were performed to examine UPFD intake relationships with lipoprotein subclasses.

In fully adjusted regression models, higher UPFD consumption was associated with reduced high-density lipoprotein (HDL) cholesterol concentrations (β = -0.024, p = 0.001), large low-density lipoprotein (LDL) levels (β = -18.645, p = 0.002), total and medium HDL concentrations (β = -0.328, p = 0.012; β = -0.510, p < 0.001), smaller LDL and HDL size (β = -0.026, p = 0.023; β = -0.023, p = 0.024), and increased medium very low-density lipoprotein levels (β = 0.053, p = 0.022), small LDL and HDL concentrations (β = 20.358, p = 0.02; β = 0.336, p = 0.011), and higher lipoprotein insulin resistance scores (β = 0.048, p = 0.012), reflecting greater lipoprotein-related insulin resistance.

Findings from this research suggest that increased intake of UPFDs is associated with a more pro-atherogenic, insulin-resistant metabolic profile in middle-to older-aged adults which may be a potential mechanism underlying reported associations between UPFD consumption and chronic disease risk and mortality.

Metabolic syndrome has become a significant public health concern. This study aims to investigate the impact of dietary patterns on metabolic syndrome in young adults and how physical activity modulates this effect. A cross-sectional study was conducted at a health management center in Tianjin, China, from September 2022 to March 2023. Participants aged 18-35 years were recruited using convenience sampling. Dietary intake was assessed using a validated food frequency questionnaire. Logistic regression models evaluated associations between these patterns and metabolic syndrome, adjusting for potential confounders. Among 442 participants, four dietary patterns were identified: Legume-Nut, Alcohol-Meat, Sugar-Processed, and Egg-Vegetable. The Legume-Nut dietary pattern was associated with a higher risk of metabolic syndrome (OR = 2.63, 95% CI: 1.08-6.37), while the Egg-Vegetable dietary pattern was associated with a lower risk (OR = 0.26, 95% CI: 0.10-0.70). No significant associations were found for the Sugar-Processed and Alcohol-Meat patterns. Subgroup analysis revealed that the Legume-Nut pattern increased the risk of metabolic syndrome among those with irregular physical activity, whereas the Egg-Vegetable pattern decreased the risk. These findings highlight the significant influence of dietary patterns on the risk of metabolic syndrome in young adults and the modifying effect of regular physical activity, underscoring the need for targeted dietary and lifestyle interventions to prevent metabolic syndrome in this population.

Lipoprotein particle concentrations and size are associated with increased risk for atherosclerosis and premature cardiovascular disease. Certain dietary behaviours may be cardioprotective and public health strategies are needed to guide consumers' dietary choices and help prevent diet-related disease. The Food Standards Agency nutrient profiling system (FSAm-NPS) constitutes the basis of the five-colour front-of-pack Nutri-Score labelling system. No study has examined FSAm-NPS index associations with a wide range of lipoprotein particle subclasses.

This was a cross-sectional study of 2006 middle-to older-aged men and women randomly selected from a large primary care centre. Individual participant FSAm-NPS dietary scores were derived from validated food frequency questionnaires. Lipoprotein particle subclass concentrations and size were determined using nuclear magnetic resonance spectroscopy. Multivariate-adjusted linear regression analyses were performed to examine FSAm-NPS relationships with lipoprotein particle subclasses.

In fully adjusted models which accounted for multiple testing, higher FSAm-NPS scores, indicating poorer dietary quality, were positively associated with intermediate-density lipoprotein (β = 0.096, p = 0.005) and small high-density lipoprotein (HDL) (β = 0.492, p = 0.006) concentrations, a lipoprotein insulin resistance score (β = 0.063, p = 0.02), reflecting greater lipoprotein-related insulin resistance, and inversely associated with HDL size (β = -0.030, p = 0.045).

A higher FSAm-NPS score is associated with a less favourable lipoprotein particle subclass profile in middle-to older-aged adults which may be a potential mechanism underlying reported health benefits of a healthy diet according to Nutri-Score rating.

Background: Obesity is a public health problem which prevalence has increased worldwide and is associated with different degrees of hemodynamic alterations and structural cardiac changes. The aim of the study is to investigate the impact of body mass index (BMI) on left atrial function using standard and advanced echocardiography in a population of patients with non-valvular atrial fibrillation (AF). Methods: 395 adult patients suffering from non-valvular AF, divided into three tertiles based on BMI value, carry out a cardiological examination with standard and advanced echocardiography. Results: Peak atrial longitudinal strain (PALS), a measure of left atrial function, is lower in the tertile with highest BMI (14.3 ± 8.2%) compared to both the first (19 ± 11.5%) and the second tertile (17.7 ± 10.6%) in a statistically significant manner (p < 0.002). Furthermore, BMI is significantly associated independent with the PALS by multilinear regression analysis, even after correction of the data for CHA2DS2-VASc score, left ventricular mass index, left ventricular ejection fraction, E/E' ratio and systolic pulmonary arterial pressure (coefficient standardized β = -0.127, p < 0.02; Cumulative R2 = 0.41, SEE = 0.8%, p < 0.0001). Conclusions: BMI could be considered an additional factor in assessing cardiovascular risk in patients with non-valvular atrial fibrillation, in addition to the well-known CHA2DS2-VASc score.

Childhood obesity rates in the UK are high. The early years of childhood are critical for establishing healthy behaviours and offer interventional opportunities. We aimed to identify studies evaluating the impact of UK-based obesity interventions in early childhood.

Systematic review using the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines.

Nine databases were searched in March 2023.

We included UK-based obesity intervention studies delivered to children aged 6 months to 5 years that had diet and/or physical activity components and reported anthropometric outcomes. The primary outcome of interest was z-score Body Mass Index (zBMI) change (within and between subjects). Studies evaluating the effects of breastfeeding interventions were not included as obesity prevention interventions, given that best-practice formula feeding is also likely to encourage healthy growth. The publication date for studies was limited to the previous 12 years (2011-23), as earlier reviews found few evaluations of interventions in the UK.

The reviewers worked independently using standardised approach to search, screen and code the included studies. Risk of bias was assessed using Cochrane tools (ROB 2 or ROBINS-I).

Six trials (five studies) were identified, including two randomised controlled trials (RCT), one cluster randomised trial (CRT), two feasibility CRTs and one impact assessment. The total number of participants was 566. Three trials focused on disadvantaged families and two included high-risk children categorised as having overweight or obesity. Compared with baseline, five interventions reported reductions in zBMI, three of which were statistically significant (p<0.05). Compared with control, five interventions showed zBMI reductions, one of which was significant. Only two trials were followed up beyond 12 months. All studies were found to have a high risk of bias. Meta-analysis was not possible due to the heterogeneity of studies.

UK evidence was limited but some interventions showed promising results in promoting healthy growth. As part of a programme of policies, interventions in the early years may have an important role in reducing the risk of childhood obesity.

CRD42021290676.

The aim of this scoping review was to map and summarise clinical trials that attempted to prevent obesity in children from birth to 7 years of age in any of the Nordic countries.

PubMed, CINAHL Plus and clinicaltrials.gov were searched for peer-reviewed papers and registered trials published in English or Swedish. The overall search period was from 1 January 2002 to 13 December 2022. We included randomised and non-randomised trials initiated from birth to 7 years of age that aimed to prevent obesity in Denmark, Finland, Iceland, Norway and Sweden.

The search resulted in 414 papers and 14 were included. Despite having diverse settings and designs, none of them reported consistently favourable results for anthropometric outcomes, apart from beneficial trends in subgroups with a high body mass index at baseline. Most studies reported temporarily improved dietary patterns.

There is a gap in the current research about how to best prevent obesity in children. We suggest that researchers should focus on risk groups and that interventions that last a number of years are needed.

Weight loss is hard to achieve and even harder to maintain. Engaging in effortful behavioural change to manage body weight can sometimes result in feelings of guilt and shame. Self-compassion, the tendency to find kindness for oneself in times of struggle, may facilitate coping with the unique challenges of weight management. This study assessed whether a remotely delivered self-compassion intervention improved weight management outcomes when delivered as a supplement to an existing digital behavioural weight management programme, Weight Watchers (WW).

Using a mixed-method study design, 249 adults seeking to manage weight were randomized to either the WW programme or WW supplemented with the self-compassion for weight management intervention (SC4WM). Participants completed measures of self-compassion, eating behaviour, physical activity, body weight and emotional well-being along with potential moderators, including weight self-stigma, eating restraint, psychological coping and perceived stress at baseline, post-intervention (4 weeks) and follow-up (12 weeks).

There was no evidence that the SC4WM intervention had a significantly different effect than WW alone. Other than body weight, all outcomes improved over time in both groups. Self-compassion was slightly higher overall in the SC4WM group (p = .05), with this group reporting higher self-kindness at 4 weeks (p = .014) and lower self-judgement at 12 weeks (p = .023) compared to the control group.

Although the SC4WM intervention group did show a small increase in self-kindness and reduction in self-judgement, weight management outcomes were not improved over and above the existing WW programme. Recommendations for adapting the SC4WM intervention to improve efficacy to augment weight management outcomes are provided.

Understanding the impacts of diets on health and the environment, as well as their association with socio-economic development, is key to operationalize and monitor food systems shifts. Here we propose a health-environment efficiency indicator defined as a ratio of health benefits and four key food-related environmental impacts (greenhouse gas emissions, scarcity-weighted water withdrawal, acidifying and eutrophying emissions) to assess how diets have performed in supporting healthy lives in relation to environmental pollution and resource consumption across 195 countries from 1990 to 2011. We find that the health-environment efficiency of each environmental input follows a nonlinear path along the Socio-Demographic Index gradient representing different development levels. Health-environment efficiency first increases thanks to the elimination of child and maternal malnutrition through greater food supply, then decreases driven by additional environmental impacts from a shift to animal products, and finally shows a slow growth in some developed countries again as they shift towards healthier diets.

Obesity is a growing pandemic with an increasing risk of inducing different cancer types, including breast cancer. Adipose tissue is proposed to be a major player in the initiation and progression of breast cancer in obese people. However, the mechanistic link between adipogenicity and tumorigenicity in breast tissues is poorly understood. We used in vitro and in vivo approaches to investigate the mechanistic relationship between obesity and the onset and progression of breast cancer. In obesity, adipose tissue expansion and remodeling are associated with increased inflammatory mediator's release and anti-inflammatory mediators' reduction.. In order to mimic the obesity micro-environment, we cultured cells in an enriched pro-inflammatory cytokine medium to which we added a low concentration of beneficial adipokines. Epithelial cells exposed to the obesity micro-environment were phenotypically transformed into mesenchymal-like cells, characterized by an increase in different mesenchymal markers and the acquisition of the major hallmarks of cancerous cells; these include sustained DNA damage, the activation of the ATR-Chk2 pathway, an increase in proliferation rate, cell invasion, and resistance to conventional chemotherapy. Transcriptomic analysis revealed that several genes, including RhoJ, CCL7, and MMP9, acted as potential major players in the observed phenomenon. The transcriptomics findings were confirmed in vitro using qRT-PCR and in vivo using high-fat-diet-fed mice. Our data suggests RhoJ as a potential novel molecular driver of tumor development in breast tissues and a mediator of cell resistance to conventional chemotherapy through PAK1 activation. These data propose that RhoJ is a potential target for therapeutic interventions in obese breast cancer patients.

The chronic consumption of caloric dense high-fat foods is a major contributor to increased body weight, obesity, and other chronic health conditions. The orbitofrontal cortex (OFC) is critical in guiding decisions about food intake and is altered with diet-induced obesity. Obese rodents have altered morphologic and synaptic electrophysiological properties in the lateral orbitofrontal cortex (lOFC). Yet the time course by which exposure to a high-fat diet (HFD) induces these changes is poorly understood. Here, male mice are exposed to either short-term (7 d) or long-term (90 d) HFD. Long-term HFD exposure increases body weight, and glucose signaling compared with short-term HFD or a standard control diet (SCD). Both short and long-term HFD exposure increased the excitability of lOFC pyramidal neurons. However, phasic and tonic GABAergic signaling was differentially altered depending on HFD exposure length, such that tonic GABAergic signaling was decreased with early exposure to the HFD and phasic signaling was changed with long-term diet exposure. Furthermore, alterations in the short-term diet exposure were transient, as removal of the diet restored electrophysiological characteristics similar to mice fed SCD, whereas long-term HFD electrophysiological changes were persistent and remained after HFD removal. Finally, we demonstrate that changes in reward devaluation occur early with diet exposure. Together, these results suggest that the duration of HFD exposure differentially alters lOFC function and provides mechanistic insights into the susceptibility of the OFC to impairments in outcome devaluation.SIGNIFICANCE STATEMENT This study provides mechanistic insight on the impact of short-term and long-term high-fat diet (HFD) exposure on GABAergic function in the lateral orbitofrontal cortex (lOFC), a region known to guide decision-making. We find short-term HFD exposure induces transient changes in firing and tonic GABA action on lOFC pyramidal neurons, whereas long-term HFD induces obesity and has lasting changes on firing, tonic GABA and inhibitory synaptic transmission onto lOFC neurons. Given that GABAergic signaling in the lOFC can influence decision-making around food, these results have important implications in present society as palatable energy dense foods are abundantly available.

To provide an update on current obesity prevalence trends and summarize the available evidence suggesting a possible plateau or stabilization in obesity rates after the previous sudden global rise.

The escalating global obesity epidemic represents one of the most serious public health challenges. There have been some indications that in high-income populations, the rate of obesity increase in adults has been stabilized after the decade 2000-2010, suggesting a possible plateau. Current evidence also suggests that obesity rates have been stabilized in children and adolescents of most economically advanced countries since 2000, which is possibly related to healthier dietary habits and increased levels of physical activity. On the other hand, there is a steady uninterrupted rise in low-income nations, and the universal trend is obesity escalation rather than slowdown, mainly driven by sharp increases in the obesity prevalence of low-income populations. Furthermore, an increasing number of high- and middle-income countries are currently experiencing an epidemic of severe obesity. In high-income populations, severe obesity is expected to double its prevalence from 10 to 20% between 2020 and 2035, posing an enormous threat for healthcare systems. Even if transiently stabilized, the obesity prevalence remains globally at unacceptably high levels, and there is no guarantee that the current stability (if any) will be maintained for long. In this review, we explore the underlying drivers of the global obesity epidemic; we provide possible explanations for the reported slowdown of the obesity rates in some countries; and we overall take a critical perspective on the obesity plateau hypothesis, emphasizing the urgent need for immediate effective actions at population and regional level in order to halt the alarming obesity escalation and its serious health risks.

Hepatosteatosis is characterized by abnormal accumulation of triglycerides (TG), leading to prolonged and chronic inflammatory infiltration. To date, there is still a lack of effective and economical therapies for hepatosteatosis. Oridonin (ORI) is a major bioactive component extracted from the traditional Chinese medicinal herb Rabdosia rubescens. In this paper, we showed that ORI exerted significant protective effects against hepatic steatosis, inflammation and fibrosis, which was dependent on LXRα signaling. It is reported that LXRα regulated lipid homeostasis between triglyceride (TG) and phosphatidylethanolamine (PE) by promoting ATGL and EPT1 expression. Therefore, we implemented the lipidomic strategy and luciferase reporter assay to verify that ORI contributed to the homeostasis of lipids via the regulation of the ATGL gene associated with TG hydrolysis and the EPT1 gene related to PE synthesis in a LXRα-dependent manner, and the results showed the TG reduction and PE elevation. In detail, hepatic TG overload and lipotoxicity were reversed after ORI treatment by modulating the ATGL and EPT1 genes, respectively. Taken together, the data provide mechanistic insights to explain the bioactivity of ORI in attenuating TG accumulation and cytotoxicity and introduce exciting opportunities for developing novel natural activators of the LXRα-ATGL/EPT1 axis for pharmacologically treating hepatosteatosis and metabolic disorders.

Obesity has reached epidemic proportion worldwide and in all ages. Available evidence points to a multifactorial pathogenesis involving gene predisposition and environmental factors. Gut microbiota plays a critical role as a major interface between external factors, i.e., diet, lifestyle, toxic chemicals, and internal mechanisms regulating energy and metabolic homeostasis, fat production and storage. A shift in microbiota composition is linked with overweight and obesity, with pathogenic mechanisms involving bacterial products and metabolites (mainly endocannabinoid-related mediators, short-chain fatty acids, bile acids, catabolites of tryptophan, lipopolysaccharides) and subsequent alterations in gut barrier, altered metabolic homeostasis, insulin resistance and chronic, low-grade inflammation. Although animal studies point to the links between an "obesogenic" microbiota and the development of different obesity phenotypes, the translational value of these results in humans is still limited by the heterogeneity among studies, the high variation of gut microbiota over time and the lack of robust longitudinal studies adequately considering inter-individual confounders. Nevertheless, available evidence underscores the existence of several genera predisposing to obesity or, conversely, to lean and metabolically health phenotype (e.g., Akkermansia muciniphila, species from genera Faecalibacterium, Alistipes, Roseburia). Further longitudinal studies using metagenomics, transcriptomics, proteomics, and metabolomics with exact characterization of confounders are needed in this field. Results must confirm that distinct genera and specific microbial-derived metabolites represent effective and precision interventions against overweight and obesity in the long-term.

Appetite can influence children's dietary choices; however, this relationship in school-aged children is still unclear. We aimed to explore the prospective associations between child appetitive traits at age 7 and food consumption at 10 years of age.

The study included 3860 children from the Generation XXI birth cohort, recruited in 2005/2006 in Porto, Portugal. The Children's Eating Behaviour Questionnaire was used to evaluate children's appetitive traits at 7 years. Food consumption was measured at 10 years through a validated Food Frequency Questionnaire. Logistic regression models were performed and adjusted for possible confounders.

Children with greater Enjoyment of Food at 7 years were 36% more likely to eat fruits ≥ 2 times/day and 54% more likely to eat vegetables > 2.5 times/day at 10 years compared to those with less frequent consumption. Children who ate more in response to negative emotions had higher odds of consuming energy-dense foods (OR = 1.33; 99% CI 1.13-1.58) and salty snacks (OR = 1.28; 99% CI 1.08-1.51) 3 years later. Those with less ability to adjust intake (higher Satiety Responsiveness) and more selective about foods (higher Food Fussiness) at 7 years were less likely to consume vegetables frequently, and were more likely to consume energy-dense foods and sugar-sweetened beverages.

Children's appetitive traits at 7 years were associated with the consumption of several food groups at 10 years of age. Eating more in response to negative emotions (Emotional Eating), with less ability to adjust intake (Satiety Responsiveness) and more food selectivity (Food Fussiness) were associated with worse dietary choices (in general, lower fruit and vegetables, and higher energy-dense foods and sugar-sweetened beverages consumption).

Level III: Evidence obtained from well-designed cohort or case-control analytic studies.

Disturbances inbody weight and adiposity in both humans and animals are met by compensatory adjustments in energy intake and energy expenditure, suggesting that body weight or fat is regulated. From a clinical viewpoint, this is likely to contribute to the difficulty that many people with obesity have in maintaining weight loss. Finding ways to modify these physiologic responses is likely to improve the long-term success of obesity treatments.

This study was designed to evaluate the long-term effects of Fructose (20%) feeding in rats, simulating metabolic syndrome (MetS), and the effects of coconut oil (C.O.) supplementation when administered in a MetS context. MetS is a cluster of systemic conditions that represent an increased chance of developing cardiovascular diseases and type 2 diabetes in the future. C.O. has been the target of media speculation, and recent studies report inconsistent results. C.O. improved glucose homeostasis and reduced fat accumulation in Fructose-fed rats while decreasing the levels of triglycerides (TGs) in the liver. C.O. supplementation also increased TGs levels and fructosamine in serum during MetS, possibly due to white adipose tissue breakdown and high fructose feeding. Pro-inflammatory cytokines IL-1β and TNF-α were also increased in rats treated with Fructose and C.O. Oxidative stress marker nitrotyrosine is increased in fructose-fed animals, and C.O. treatment did not prevent this damage. No significant changes were observed in lipoperoxidation marker 4-Hydroxynonenal; however, fructose feeding increased total conjugated dienes and caused conjugated dienes to switch their conformation from cis-trans to trans-trans, which was not prevented by C.O. treatment. Potential benefits of C.O. have been reported with inconsistent results, and indeed we observed some benefits of C.O. supplementation in aiding weight loss, fat accumulation, and improving glucose homeostasis. Nonetheless, we also demonstrated that long-term C.O. supplementation could present some problematic effects with higher risk for individuals suffering MetS, including increased TGs and fructosamine levels and conformational changes in dienes.

Alcohol is calorie dense, but unlike food products, alcoholic drinks tend to be exempt from nutritional labelling laws that require energy content information to be displayed on packaging or at point of purchase. This review provides a perspective on the likely efficacy of alcoholic drink energy labelling as a public health policy to reduce obesity and discusses key questions to be addressed by future research. First, the contribution that alcohol makes to population level daily energy intake and obesity is outlined. Next, consumer need for alcohol energy labelling and the potential impacts on both consumer and industry behavior are discussed. Pathways and mechanisms by which energy labelling of alcoholic drinks could reduce obesity are considered, as well as possible unintended consequences of alcoholic drink energy labelling. Would widespread energy labelling of alcoholic drinks reduce obesity? The unclear effect that alcohol has on population level obesity, the modest contribution calories from alcohol make to daily energy intake and limited impact nutritional labelling policies tend to have on behavior, suggest alcohol energy labelling may have limited impact on population obesity prevalence as a standalone policy. However, there are a number of questions that will need to be answered by future research to make definitive conclusions on the potential for alcohol energy labelling policies to reduce obesity.

Policy Points Between 1998 and 2016, 24 states and the District of Columbia passed laws meant to increase the time that children spent in physical education (PE) or other school-based physical activity (PA). Schools largely disregarded changes to PE/PA laws, which did not increase the time that children spent in PE or recess and did not reduce body mass index, overweight, or obesity. Closer oversight of schools would be needed to improve compliance with state PE and PA laws. Yet, even with better compliance, we estimate that PE and PA policies would be inadequate to reverse the obesity epidemic. Policies should also address consumption, both inside and outside of school.

To control childhood obesity, leading medical organizations have recommended increasing the time that children spend in physical education (PE) and other school-based physical activity (PA). Yet, it is unknown how many states have passed laws that codify these recommendations, and it is unknown what effect changing state laws has had on obesity or the time that children actually spent in PE and PA.

We joined state laws to national samples of 13,920 children from two different cohorts of elementary students. One cohort attended kindergarten in 1998; the other attended kindergarten in 2010; both cohorts were followed from kindergarten through fifth grade. We estimated the effects of changes to state laws in a regression with state and year fixed effects.

Twenty-four states and the District of Columbia increased the time that children were recommended or required to spend in PE or PA. These changes in state policies did not increase actual time spent in PE or recess, did not affect average body mass index (BMI) or BMI Z score, and did not affect the prevalence of overweight or obesity.

Increasing the PE or PA time required or recommended by state laws has not slowed the obesity epidemic. Many schools have failed to comply with state laws. A back-of-the-envelope calculation suggests that, even with better compliance, the legislated changes in PE laws might not have changed energy balance enough to reduce obesity prevalence.

We examined the association of changes in physical activity and diet with obesity development and changes in body fat percentage, body mass index, and waist circumference. 31,344 adults without obesity at baseline (age = 56.0 ± 7.5 years; female = 49.1%) from the UK Biobank were included. Physical activity was categorised based on public health guidelines as: inactive; insufficient; and sufficient. Diet category was assigned based on an established composited score that included consumption of fruits, vegetables, fish, red meat (unprocessed), and processed meat. Diet was categorised as: poor; reasonable; and good. Physical activity and diet changes were categorised based on changes in category: worsened; stable; increased (physical activity)/improved (diet). During a mean follow up of 6.8 (SD = ±2.3) years, 1354 (4.3%) participants developed obesity. Compared to stable physical activity-diet, increasing physical activity was associated with the lowest obesity odds, across diet changes (e.g., OR [95%CI]: diet worsened (0.89 [0.69, 1.15]); diet improved (0.65 [0.48, 0.89])). Increasing physical activity with improved diet was associated with the largest difference in body fat percentage (β:-0.62 [-0.82, -0.41]), body mass index (-0.37 [-0.47, -0.28]), and waist circumference (-1.21 [-1.63, -0.79]). Excluding adults with a history of smoking, or major illness, lowered obesity odds among participants with increased physical activity by an additional 11%-21%. In those who decreased physical activity obesity was attenuated when combined with diet improvement. Improvements in physical activity or diet mutually attenuated the deleterious associations of the other behaviour's deterioration. In most analyses, increases in physical activity conferred consistent positive associations against the development of obesity, across dietary change groups.

Obesity presents a significant public health problem. Brain plays a central role in etiology and maintenance of obesity. Prior neuroimaging studies have found that individuals with obesity exhibit altered neural responses to images of food within the brain reward system and related brain networks. However, little is known about the dynamics of these neural responses or their relationship to later weight change. In particular, it is unknown if in obesity, the altered reward response to food images emerges early and automatically, or later, in the controlled stage of processing. It also remains unclear if the pretreatment reward system reactivity to food images is predictive of subsequent weight loss intervention outcome.

In this study, we presented high-calorie and low-calorie food, and nonfood images to individuals with obesity, who were then prescribed lifestyle changes, and matched normal-weight controls, and examined neural reactivity using magnetoencephalography (MEG). We performed whole-brain analysis to explore and characterize large-scale dynamics of brain systems affected in obesity, and tested two specific hypotheses: (1) in obese individuals, the altered reward system reactivity to food images occurs early and automatically, and (2) pretreatment reward system reactivity predicts the outcome of lifestyle weight loss intervention, with reduced activity associated with successful weight loss.

We identified a distributed set of brain regions and their precise temporal dynamics that showed altered response patterns in obesity. Specifically, we found reduced neural reactivity to food images in brain networks of reward and cognitive control, and elevated reactivity in regions of attentional control and visual processing. The hypoactivity in reward system emerged early, in the automatic stage of processing (< 150 ms post-stimulus). Reduced reward and attention responsivity, and elevated neural cognitive control were predictive of weight loss after six months in treatment.

In summary, we have identified, for the first time with high temporal resolution, the large-scale dynamics of brain reactivity to food images in obese versus normal-weight individuals, and have confirmed both our hypotheses. These findings have important implications for our understanding of neurocognition and eating behavior in obesity, and can facilitate development of novel integrated treatment strategies, including tailored cognitive-behavioral and pharmacological therapies.

There are well documented socioeconomic disparities in diet quality and obesity. Menu energy labelling is a public health policy designed to improve diet and reduce obesity. However, it is unclear whether the impact energy labelling has on consumer behaviour is socially equitable or differs based on socioeconomic position (SEP).

Systematic review and meta-analysis of experimental (between-subjects) and pre-post implementation field studies examining the impact of menu energy labelling on energy content of food and/or drink selections in higher vs. lower SEP groups.

Seventeen studies were eligible for inclusion. Meta-analyses of 13 experimental studies that predominantly examined hypothetical food and drink choices showed that energy labelling tended to be associated with a small reduction in energy content of selections that did not differ based on participant SEP (X2(1) = 0.26, p = .610). Effect estimates for higher SEP SMD = 0.067 [95% CI: -0.092 to 0.226] and lower SEP SMD = 0.115 [95% CI: -0.006 to 0.237] were similar. A meta-analysis of 3 pre-post implementation studies of energy labelling in the real world showed that the effect energy labelling had on consumer behaviour did not significantly differ based on SEP (X2(1) = 0.22, p = .636). In higher SEP the effect was SMD = 0.032 [95% CI: -0.053 to 0.117] and in lower SEP the effect was SMD = -0.005 [95% CI: -0.051 to 0.041].

Overall there was no convincing evidence that the effect energy labelling has on consumer behaviour significantly differs based on SEP. Further research examining multiple indicators of SEP and quantifying the long-term effects of energy labelling on consumer behaviour in real-world settings is now required.

Registered on PROSPERO (CRD42022312532) and OSF ( https://doi.org/10.17605/OSF.IO/W7RDB ).

Normal weight obesity (NWO) describes individuals who have a normal weight body mass index (BMI), but have an unhealthy amount of body fat. Based on the life-long habits that develop during college, exploring NWO among a college-aged population may be essential in identifying and preventing obesity that develops in early adulthood. This study aimed to characterize NWO among young adults with normal weight BMI. 94 college students (Mean ± SD: Age: 19.6 ± 1.5 yrs; BMI: 21.9 ± 1.8 kg/m²) enrolled during the Fall semester (Aug-Oct) were assessed for body composition by dual energy X-ray absorptiometry to determine body fat percentage, fat mass, lean mass and trunk fat; lifestyle habits were characterized from validated questionnaires. Mean arterial pressure and metabolic biomarkers [total cholesterol, high density lipoproteins, non-high density lipoproteins, and glucose] were evaluated for cardiometabolic health. NWO was defined using data from the National Health and Nutrition Examination Survey (NHANES) for body fat percentage. Data was analyzed by group (NWO vs NWL) and sex. with independent t-tests to investigate continuous data, and chi-square test of independence for categorical data. Rates of NWO for the total sample were 13.8%. Males (n=30) had a higher rate of NWO (26.7%) compared to females (n=64; 7.8%). NWO individuals had higher fat mass (p=0.024), trunk fat (p<0.001), and larger waist to hip ratio (p<0.001) than normal weight lean. NWO also engaged in less vigorous physical activity (p=0.043). The occurrence of NWO among otherwise healthy college students is evident. Identification of these individuals may be an effective component for obesity prevention and treatment. Determining feasible methods to measure body fat in this population is essential, as BMI may mask obesity in a young adult population.

The lateral orbitofrontal cortex (lOFC) receives sensory information about food and integrates these signals with expected outcomes to guide future actions, and thus may play a key role in a distributed network of neural circuits that regulate feeding behavior. Here, we reveal a new role for the lOFC in the cognitive control of behavior in obesity. Food-seeking behavior is biased in obesity such that in male obese mice, behaviors are less flexible to changes in the perceived value of the outcome. Obesity is associated with reduced lOFC inhibitory drive and chemogenetic reduction in GABAergic neurotransmission in the lOFC induces obesity-like impairments in goal-directed behavior. Conversely, pharmacological or optogenetic restoration of inhibitory neurotransmission in the lOFC of obese mice reinstates flexible behavior. Our results indicate that obesity-induced disinhibition of the lOFC leads to a failure to update changes in the value of food with satiety, which in turn may influence how individuals make decisions in an obesogenic environment.

Naringin, a flavonoid present in citrus fruits, has been known for the capacity to reduce lipid synthesis and anti-inflammatory. In this study, we investigated whether naringin increases lipolysis and fatty acid β-oxidation to change fat deposition.

In in vivo experiment, obese adult mice (20-weeks-old, n = 18) were divided into control group fed with normal diet and naringin-treated group fed with naringin-supplemented diet (5 g/kg) for 60 days, respectively. In in vitro experiment, differentiated 3T3-L1 adipocytes were treated for four days with or without naringin (100 µg/mL).

Supplementing naringin significantly reduced the body weight, abdominal fat weight, blood total cholesterol content of mice, but did not affect food intake. In addition, naringin decreased levels of pro-inflammatory factors in adipose tissue including interleukin-1β (IL-1β), interleukin-6 (IL-6), and monocyte chemotactic protein 1 (MCP-1). Naringin increased the expression of AMP-activated protein kinase (AMPK), a key factor in cellular energy metabolism, and raised the ratio of p-AMPK/AMPK in mouse liver tissue. The protein expression of hormone-sensitive lipase (HSL), phospho-HSL563 (p-HSL563), p-HSL563/HSL, and adipocyte triglyceride lipase (ATGL) was significantly increased in the adipose tissue of naringin-treated mice. Furthermore, naringin enhanced the expression of fatty acid β-oxidation genes, including carnitine palmitoyl transferase 1 (CPT1), uncoupling protein 2 (UCP2), and acyl-coenzyme A oxidase 1 (AOX1) in mouse adipose tissue. In in vitro experiment, similar findings were observed in differentiated 3T3-L1 adipocytes with naringin treatment. The treatment remarkably reduced intracellular lipid content, increased the number of mitochondria and promoted the gene expression of HSL, ATGL, CPT1, AOX1, and UCP2 and the phosphorylation of HSL protein.

Naringin reduced body fat in obese mice and lipid content in differentiated 3T3-L1 adipocytes, which was associated with enhanced AMPK activation and upregulation of the expression of the lipolytic genes HSL, ATGL, and β-oxidation genes CPT1, AOX1, and UCP2.

Due to the growing global trend of obesity, it is necessary to study the diet quality as a modifiable factor to reduce the dangerous consequences of obesity. Therefore, the aim of this study was to evaluate the association between meal-based diet quality index-international (DQI-I) with obesity in adults.

This cross-sectional study was performed on 850 men and women in Tehran (aged 20-59 y). Dietary intakes were assessed using three 24-h dietary recalls. Meal-based Diet quality was assessed based on the construction of DQI-I. The total DQI-I score ranged from 0 to 100, with higher scores denoting better diet quality. Multiple linear regression analysis was used to examine the association of DQI-I and BMI in each meal and Logistic regression analysis was used to examine the association of DQI-I and obesity in each meal.

The mean (± SD) of age, body mass index (BMI), waist circumference (WC) and waist to hip ratio (WHR) were 42.35(± 10.90) years, 27.32(± 5.61) kg/m2, 89.09 (± 12.04) cm and 0.86 (± 0.11), respectively. In none of the meals, after adjusting for confounders, no significant difference in BMI was observed in the both women and men groups. After controlling of confounders, there was not any relationship between meal-based DQI-I and BMI resulted from multiple linear regression analysis also there was not any significant association between meal-based DQI-I and obesity resulted from Logistic regression analysis.

In this study, we did not find any significant association between meal-specified DQI with obesity. To reach the better evaluation, more prospective studies with large sample size are needed.