Appetite

Background Homeostatic and hedonic brain circuits regulate eating behavior but also shape how food memories are encoded and retrieved. Objective We examined neural correlates during food memory encoding and retrieval during functional MRI before and after a 14-day prebiotic intervention in a preregistered, double-blind crossover trial (NCT03829189). Design 55 healthy adults with overweight (19 females, age 28{+/-}6.5, BMI 25-30 kg/m2) underwent 3 Tesla task-based functional MRI before and after dietary intervention of prebiotic (30g inulin/day) or equicaloric placebo for 14 days. Peripheral metabolic, short-chain fatty acids (SCFA), and microbial markers using 16S rRNA analysis were assessed in fasting blood and feces. Results Food memory was enhanced by assigned reward value and engaged brain activity in hedonic regions, including the nucleus accumbens, orbitofrontal cortex, caudate, cingulate, dorsomedial prefrontal cortex, and ventral tegmental area, as well as homeostatic and memory-related such as the hypothalamus and the hippocampus. Higher neural activations during food encoding were related to higher Actinobacteriota abundance, fecal SCFA acetate, and creatinine levels, and lower ghrelin levels. Activations in reward-related and homeostatic brain areas partially correlated with insulin, glucagon-like peptide-1, leptin, and thyroid-stimulating hormone levels. Neural activations related to food memory decreased after prebiotic intervention. The prebiotic supplementation induced decrease of hippocampal activity during food encoding related to changes in gut microbiota Firmicutes abundance. Conclusions This study indicates that neuronal food-related memory processes depend on homeostatic and hedonic brain signals modulated by the gut-brain axis. Our findings raise implications for the treatment of obesity and substance use disorder.

Unpredictable and insufficient access to food, known as food insecurity, is associated with the development of obesity. However, causal mechanisms underlying this paradoxical relationship remain poorly understood. Using a rat model of food insecurity, this study investigated whether food insecurity causes dysregulated feeding behaviours, specifically impaired gut signal sensitivity and enhanced cue-driven appetitive responses. Adolescent female rats were assigned to receive either ad libitum chow access (Food secure), 90% caloric restriction (Food restricted) or unpredictable quantity and timing of food access (Food insecure), for 4 weeks. After which, rats were returned to an ad libitum chow diet for the remainder of the study. To examine gut signal sensitivity, we measured the effects of cholecystokinin (CCK) on 10% sucrose intake. To examine cue-driven feeding behaviours, we used Pavlovian appetitive conditioning and measured appetitive responses towards a food-predictive cue. Results showed that prior food insecure rats were less sensitive to the intake inhibitory effects of CCK and exhibited enhanced cue-induced appetitive behaviours, when compared to food secure and food restricted groups. Anxiety-like behaviours or learning and memory was not different between groups. At the end of the study, adolescent caloric restriction resulted in reduced fat mass, plasma leptin levels and body weight when compared to food secure, but not food insecure rats, suggesting that adolescent food insecurity somewhat overcame these metabolic effects. Taken together, our findings suggest that adolescent food insecurity impaired gut signal sensitivity and heightened food cue sensitivity, which may cause enduring metabolic and behavioural adaptations that promote overeating and weight gain.

Although dietary intake is a leading risk factor for many common diseases, adherence to dietary recommendations remains low. This may partly reflect limited consideration of individual differences in eating behavior that arise from both environmental and genetic factors. While genome-wide association studies (GWAS) of dietary intake have identified hundreds of associated loci, the X chromosome has largely been ignored. To address this gap, we applied multiple X-chromosome-wide association study (X-WAS) models on dietary intake phenotypes to identify novel associations. We performed X-WAS of 46 dietary intake traits from food frequency questionnaires in up to 424,758 European participants from the UK Biobank. Phenotypes included quantitative measures (e.g., fruit intake), binary traits (e.g., decaffeinated vs caffeinated coffee), and principal component-derived food groups. We tested for genetic associations using several models: a traditional sex-combined additive GWAS, additive models stratified by sex, and two joint models accounting for sex-interaction effects and non-additivity. We also conducted X-WAS in five additional genetic ancestry groups and performed a sex-combined multi-ancestry additive GWAS meta-analysis with up to 445,773 individuals. We identified 18 loci associated with 20 dietary intake traits (P < 5x10-8), including 17 variants without prior associations in the GWAS Catalog. Among these loci, 10 were significant across multiple X-WAS models, and 5 were strongest in a model other than the traditional sex-combined additive GWAS, highlighting the value of approaches that address known complexities of the X chromosome. These results demonstrate that incorporating the X chromosome in GWAS can reveal novel loci, even for complex behavioral traits such as dietary intake. Applying multiple association models further improves discovery by accounting for unique features of the X chromosome. Author SummaryAlthough diet is a major risk factor for many common diseases, adherence to healthy eating guidelines remains low. One reason is that current recommendations do not account for individual differences in food choice that arise from environmental or genetic factors. Previous genetic studies have identified hundreds of genetic variants associated with dietary behaviors, but most have excluded the X chromosome due to its analytical complexity and differences between males and females. However, accumulating evidence suggests that the X chromosome contains important genetic variation that impacts complex traits. We analyzed data from hundreds of thousands of individuals to identify genetic variants on the X chromosome associated with dietary intake. To address the unique features of the X chromosome, we applied multiple different models that account for sex-differences and non-additive genetic effects. We identified 18 regions in the genome associated with at least one dietary intake trait. These results reveal new insights into the genetics underlying eating behavior and highlight the importance of incorporating the X chromosome in genetic studies of complex traits.

Obesity is associated with low-grade inflammation, which - our prior work shows - causally and reversibly increases effort aversion and related brain responses during food-related decision-making. However, how these laboratory findings translate to daily-life (food) motivation remains unclear. This study investigated low-grade inflammation in more ecologically valid measures of (food-related) motivation in obesity. We conducted a cross-sectional study (N=145 women, BMI>27 kg/m2, 18-59 yrs) and a 12-week randomized controlled trial (N=57 women, BMI>30 kg/m2, 18-59 years, C-reactive protein (CPR)>3 mg/l) testing the anti-inflammatory drug colchicine versus placebo. We measured effort-related food intake using a bogus taste test, daily-life motivation using ecological momentary assessment (EMA), and dietary intake using a food frequency questionnaire (FFQ). INFLA-score (CRP, white blood cell count, neutrophil-to-lymphocyte ratio, platelets) related to lower intake of high-effort food items on the taste test ({beta} -0.26 SD, p=0.011), lower engagement in high-effort activities (OR 0.72, p<0.001), and negatively moderated the association between anticipation and activity completion in EMA (OR 0.89, p=0.032). On the FFQ, INFLA-score related to lower intake of legumes and fruits and more intake of processed meat (all p<0.05). Colchicine decreased overall caloric intake ({beta} -341 kcal, p=0.018). A decrease in inflammation related to healthier dietary choices (Spearman {rho}=0.37, p=0.013). Colchicine did not affect effort-related food intake on the taste test or EMA. These findings indicate that that obesity-related inflammation is associated with increased effort-related food intake and motivation in daily life, and that reducing inflammation decreases (unhealthy) food intake. Such effects may partly underlie the challenges of achieving and maintaining weight loss.

ObjectiveThe average American consumes 55% of their daily energy from ultraprocessed foods (UPF) created through industrial processes and additives not used at home. We investigated if a high-UPF diet alters brain response to milkshake compared with a diet free-from UPF (NonUPF) in emerging adults, who are in a critical period for brain development and typically consume high amounts of UPF. MethodsIn a randomized controlled crossover trial participants aged 18-25 completed two, 2-week controlled feeding periods including a UPF (81% UPF) and nonUPF (0% UPF) diet. Before and after each diet intervention participants consumed milkshake concomitant with functional magnetic resonance imaging. ResultsIn the entire cohort, there were no differences between diet conditions in brain response. An exploratory analysis revealed orbitofrontal cortex (OFC) response to milkshake decreased after the UPF diet and increased following the NonUPF diet in adolescents (18-21 years) but not young adults (22-25 years). Habitual UPF intake (gs) was positively associated with OFC response to milkshake independent of diet intervention in all participants. ConclusionsAn acute UPF dietary intervention may only alter brain response in adolescents. Further work is needed to determine potential vulnerability of adolescents to changes in dietary UPF on brain response to rewards.

Objective: Studies assessing the validity of screening measures for avoidant/restrictive food intake disorder (ARFID) remain scarce. We evaluated the diagnostic performance and validity of an online, parent-reported screening approach for ARFID in a population-based sample of children. Methods: Participants were drawn from the ARFID Initiative Sweden (ARIES) cohort and included 65 children aged 6-14 years. Parents completed three screening questionnaires (Pica, ARFID, and Rumination Disorder Interview-ARFID Questionnaire [PARDI-AR-Q], Nine-Item ARFID Screen [NIAS], and Parent Eating Disorder Examination Questionnaire [PEDE-Q]), followed by a diagnostic interview (PARDI). Diagnostic performance indices (sensitivity, specificity, positive predictive value [PPV], and negative predictive value [NPV]) were calculated. Convergent validity was assessed via correlations between questionnaire and interview dimensions. Results: The combined screening algorithm demonstrated perfect sensitivity and NPV, indicating accurate detection of all ARFID cases and exclusion of non-cases. Specificity was high (0.83), and PPVs ranged from 0.91 to 0.95, decreasing to 0.78 under a more conservative operationalization of ARFID Criterion A4 (psychosocial impairment). Diagnostic performance varied across ARFID criteria: PPVs were low for medically anchored Criteria A1-A3 but high for Criterion A4 (psychosocial impairment; PPV=0.95). Correlations between screening measures and corresponding interview dimensions were generally moderate to strong, supporting convergent validity. Children meeting threshold ARFID criteria showed significantly greater symptom severity than subthreshold cases at screening. Discussion: These findings support the use of a multi-instrument, parent-reported screening approach for ARFID in large-scale pediatric research and highlight the centrality of psychosocial impairment, underscoring the need for standardized operationalization of this criterion.

Background: Childhood obesity is a prevalent public health concern, particularly among children from marginalized backgrounds. Epigenomic mechanisms, including DNA methylation (DNAm), offer insight into the biological embedding of metabolic risk, yet protective family-level factors remain understudied. This study examined whether participation in a positive parenting intervention was associated with reduced epigenetic cardiometabolic risk among preschool-aged children. Methods: Participants were 74 children (n = 35 intervention; n = 39 services-as-usual; mean age = 36 months). Using a secondary analysis of a randomized controlled trial, DNAm-derived body mass index (BMI) and anthropometric BMI were assessed at baseline and 12-month follow-up, and parenting practices were observed post-treatment. Results: Children in the intervention group demonstrated significantly lower DNAm BMI at 12 months relative to controls, adjusting for child sex, race and/or ethnicity, and anthropometric BMI. No treatment effect was observed for anthropometric BMI, and DNAm BMI was not associated with anthropometric BMI at 12 months. Although parenting practices improved, they did not mediate intervention effects on DNAm-derived BMI. Conclusions: Parenting interventions may influence biological pathways related to cardiometabolic risk, even before changes in anthropometric outcomes, underscoring the potential of family-centered approaches to promote early metabolic health.

Adolescence is a sensitive period during which unhealthy diets may shape metabolic health and cognition. Diets high in fat and sugar have been linked to obesity, impaired glucose regulation and hippocampus-dependent deficits, but the exposure duration required to affect cognition remains unclear. This study examined whether adolescent-onset exposure to a high-fat high-sucrose (HFHS) diet induces metabolic dysfunction and impairs object-based memory, spatial working memory and spatial pattern separation in male Long Evans rats. Rats were assigned to a control or HFHS diet at four weeks of age and remained on this diet into adulthood. Basal blood glucose was assessed monthly and home-cage behaviour using 48-hour LABORAS recordings. Cognitive testing started after 10 weeks of diet exposure, when basal glucose was elevated in HFHS-fed rats. Object displacement and novel object recognition were used in short open-field test settings, whereas touchscreen-based trial-unique nonmatching-to-location testing (TUNL) assessed spatial working memory and pattern separation across repeated operant sessions. Finally, glucose (in)tolerance and tissue weights were measured. HFHS diet exposure produced a metabolic phenotype, including increased body weight, elevated basal glucose, impaired glucose tolerance and increased liver and gonadal white adipose tissue weights. The diet also altered the general behavioural repertoire, with increased immobility and grooming and reduced rearing. HFHS-fed rats did not differ from controls in object displacement or novel object recognition performance. In the touchscreen task, both groups acquired the task at a comparable rate. Long-delay and spatial separation challenges reduced performance as expected, confirming task sensitivity, but did not reveal diet-related impairments. These findings show that adolescent-onset HFHS diet exposure induces metabolic dysfunction but does not necessarily produce detectable cognitive impairment when behavioural testing starts after 10 weeks of exposure. Longer exposure or advanced diet-induced inflammatory or neurobiological alterations may be required to reveal cognitive consequences.

Objective: This systematic review and meta-analysis examined 1) the effects of stress management interventions on changes in stress eating for women, and 2) the longevity of these effects, by summarizing and assessing evidence from controlled and non-equivalent pretest-posttest intervention studies. Method: Five databases (PsycINFO, PubMed, Medline, Web of Science, CINAHL), existing sources, and grey literature were searched (February - June 2025). Studies that assessed stress eating or emotional eating, included a stress management intervention, and comprised at least 70% women were included. The primary outcome was reduction in stress eating. Data were pooled in meta-analyses using multi-level random-effects models and subset by follow-up period. Risk of bias was assessed via funnel plots and sensitivity analyses. Results: Sixty studies with 119 effect size estimates were included in the primary analysis. Pooled estimates indicated that stress management interventions significantly reduced stress eating (Hedges g = -0.4174, p < 0.001), with pre-post designs having larger effects than controlled trials. Subgroup analyses of follow-up periods found small effects in the short-term (before 3 months; Hedges g = -0.4202, p < 0.0001) and moderate effects for mid-term (3-6 months; Hedges g = -0.5886, p < 0.0001). Effects beyond 6 months were small and nonsignificant (Hedges g = -0.4370, p = 0.0660). Conclusion and Relevance: Stress management interventions appear to be effective for reducing stress eating for women, suggesting the potential to incorporate stress management in interventions targeting obesity. Effects may be only sustained 6 months post-intervention, suggesting the need for strategies to bolster long-term effectiveness.

Of the three dietary macronutrients, protein plays an especially pivotal role in physiological functions. Nevertheless, the behavioural control of protein intake is poorly understood. In this study, we used Feeding Experimentation Devices (FED3s) to examine the structure of ingestive behaviour in mice given access to diets varying in protein content. Adult C57BL/6NRj mice were contact-housed in pairs in custom-made cages with perforated dividers, each having access to an individual FED3 unit. Mice were given ad libitum access to either 20 mg control, non-restricted (NR) pellets (20% casein) or 20 mg protein-restricted (PR) pellets (5% casein) from FED3s on free-feeding mode. Each pellet retrieval event was timestamped ~24 h/day. All mice experienced both diets for 7 days with order of diet presentation counterbalanced (i.e., NR[-&gt;]PR and PR[-&gt;]NR). Analysis of dynamics of pellet intake per day revealed that mice that were initially protein-restricted first showed a decrease in pellet intake before increasing on later days and exhibiting a persistent high level of intake once non-restricted diet was available. The group that was initially non-restricted exhibited a blunted response to the same diet manipulation. In addition, we clustered pellet retrieval data into discrete clusters of feeding events and used a mathematical approach to determine the boundary of meals (2-5 pellets), separated from "snacks" (1 pellet) and "feasts" (>5 pellets). We identified alterations in meal patterning in response to diet manipulation with protein restriction increasing "snacking" and leading to increased meal number, and reduced meal size. Moreover, restored access to NR diet, elicited "feasting". These effects depended on the sequence of diets the mice experienced, such that the effects were stronger in initially protein restricted mice compared to those initially non-restricted. In summary, our findings show that manipulation of dietary protein levels affects meal patterning in adult mice.

Understanding how nutritional interventions alter food evaluations may help clarify mechanisms of dietary behavior change; however, most studies focus on intake outcomes and rarely assess within-person changes in subjective food evaluation. We developed a brief, image-based rating tool that measures two core dimensions of food evaluation, liking and perceived healthiness, using standardized food images. The tool was piloted in adults with type 2 diabetes participating in a medically supervised intervention that included structured glucose monitoring and professional dietary guidance. Ratings were collected at baseline, post-monitoring, and follow-up. In line with the methodological aim of this study, we examined whether the tool demonstrates internal coherence, sensitivity to change, and external validity against expert ratings and physiological measures, and whether it can capture item-level patterns relevant to eating behavior. Results provide preliminary evidence that the tool is feasible, it is low-burden, and capable of detecting coherent relationships between food liking and health perceptions, including coordinated within-person changes over time and meaningful associations with external benchmarks. To support scalability and self-administration, we also developed an online smartphone-based demonstration version to exemplify the task structure and user experience. Overall, this pilot study suggests that a short, flexible rating task can serve as a practical measurement tool for tracking intervention-relevant changes in food evaluation and for informing the design of future nutritional interventions.

Considerable evidence suggests that the motivational control of instrumental action depends on incentive learning; i.e., on the opportunity to learn how the value of the consequences or outcome of an action, (e.g., a specific food) varies under different motivational conditions (e.g., under different degrees of hunger). The current study investigated whether learning the values of high-protein and high-carbohydrate rewards under different degrees of protein and carbohydrate appetite is also necessary for these nutrient-specific appetites to exert control over instrumental performance. Experiment 1 gave differing consummatory experience to whey protein and polycose carbohydrate outcomes under protein and carbohydrate appetite and found that, without the opportunity for incentive learning, the performance of actions earning these outcomes was insensitive to a shift in appetite. However, once the opportunity for incentive learning was provided, the rats increased their instrumental performance on a lever that earned the whey outcome relative to the polycose lever when protein hungry and on the polycose lever relative to the whey lever when carbohydrate hungry. Experiment 2 assessed how these nutrient-specific states exerted this control; whether, once learned, nutrient values were immediately controlled by nutrient appetite or whether this was based on conditional control acquired during experience with the outcomes under different nutrient appetites. We found that exposure to an outcome under a single nutrient-specific state was not sufficient to establish state-specific control. Instead, establishing the conditional control of outcome value required exposure to both the whey and polycose outcomes under both protein and carbohydrate appetites.

Background: Black adults bear a disproportionate burden of cardiometabolic dysfunction, yet most dietary trial evidence comes from predominantly White cohorts. Objective: To evaluate whether a personalized whole-food dietary intervention improves cardiometabolic outcomes more in Black than White young adults with overweight or obesity. Methods: In this 8-week randomized, controlled trial (ClinicalTrials.gov: NCT04635917), 112 Black and White adults (18-35 years; BMI 25-45 kg/m2) were block-randomized by race to a personalized dietary intervention providing whole foods (PD, n=57) or conventional dietary counseling at baseline (BL) using MyPlate guidelines (CD, n=55). Primary outcomes were Matsuda Index and fasting and OGTT-derived glucose, insulin, and non-esterified fatty acids. Other glucoregulatory, cardiovascular, anthropometric, appetite, and cognitive outcomes were also assessed. Outcomes were analyzed using baseline-adjusted linear models with sensitivity analyses adjusting for baseline BMI and food security score. Results: Compliance with study food consumption was 85-91%. Diet quality was higher in PD than CD (P < 0.05), with larger gains in vegetable-related outcomes among Black participants (group x race, P < 0.05). HOMA-{beta} was lower in PD than CD overall (P < 0.05). In sensitivity analyses, Black PD participants had greater fasting insulin reductions than White, especially in the latter half of intervention (week x group x race, P < 0.05), with a similar tendency for HOMA-IR. Glucose AUC 0-30 min was higher in White than Black PD participants (group x race, P < 0.05). Concentration performance was higher in PD than CD overall (P < 0.05), with larger gains in processing speed and accuracy among Black than White participants (group x race, P < 0.05). No effects were observed for cardiovascular or appetite outcomes. Conclusions: The personalized whole-food intervention produced differential effects in fasting insulin and early-phase glucose handling, and greater benefits in attention, in Black compared with White young adults with overweight or obesity during weight maintenance.

Background: Despite growing evidence that personalised nutrition (PN) can improve dietary behaviour and health outcomes, the implementation of PN food services in real-world settings remains largely unexplored. This study evaluated the feasibility of a comprehensive PN service for delivering personalised nutrition products (PNPs) in a military setting and assessed consumer acceptance following repeated consumption. Methods: A complete PN service was developed to design, produce, and distribute personalised nutrition products (PNPs). Twenty-five participants from the Royal Netherlands Army took part in a feasibility study, using a single-cohort pre-test post-test design. Each participant consumed a PNP on 10 consecutive days during a two-week combat training exercise. Product liking was assessed through daily questionnaires, while broader user experiences were assessed at baseline (t=0), one week follow-up (t=1) and two-week endline (t=2). Results: The PN service was succesfully implemented during a real-life military training exercise. In total, 229 PNPs were produced and distributed. Participants evaluated all aspects of the PN service from just below neutral to slightly positive (3.4 to 5.0 on 7 point scales). Across the different product combinations, mean overall liking and all sensory attributes were slightly positive (5.7 to 6.1 on 9 point scales). Overall liking did not change over time (F (9,194) = 1.242, p=0.27). Attitudes toward a PNP service in the army decreased over time, but remained just-above neutral at study end. Conclusions: This study demonstrates the feasibility of a personalised nutrition service in a military setting. Both the service and PNPs received modestly positive evaluations, while repeated exposure did not change overall liking of the products. Although further optimisation of the service is warranted, these findings support the potential for broader implementation of PN services in military and other high performance environments.

Background: 39M children worldwide are overweight or have obesity, accelerating risk for adult non-communicable diseases. Presently, interventions to prevent obesity have had limited success due to poor timing and lack of personalisation. Objective: We aimed to identify early-life predictors of childhood obesity (ChOB) that could aid targeting specific population subsets for obesity prevention interventional studies. Methods: Data were from the Raine Study Gen2 participants (n=1494). Anthropometric and genetic predictors evaluated included birthweight (BW), early-life BMI (1-3 years), and three polygenic scores (PGS) [two BW-PGSs (BW-PGS2016 and BW-PGS2019) and a ChOB-PGS], developed from BW and ChOB genome-wide-association-studies, respectively. Multivariate analyses were performed to investigate associations between predictors and child-BMI (5-, 8-, 10-years). Results: BW-PGS2019 associate with child-BMI at 5-years. BW-PGS2016 was not associated with child-BMI. Remaining predictors positively associate with child-BMI at 5-, 8- and 10-years (p<0.001). Early-life BMI, ChOB-PGS and BW accounted for up to 38.7%, 5.8% and 3.4% of the variability in child-BMI, respectively. Conclusions: Our data suggest early-life BMI is a better predictor of child-BMI than ChOB-PGS, and BW, accounting for up to ten-fold more variance in child-BMI. Future interventional studies to mitigate obesity could target early-life BMI as a marker to identify children at the highest risk.

Objectives: Estimate the prevalence and sociodemographic correlates of adolescent-reported food insecurity experiences from 2019-2021. Methods: Repeat cross-sectional data were collected in November-December 2019, 2020, and 2021 from adolescents aged 10-17 years living in the ten Canadian provinces (n = 11,057). The prevalence of ten items and five food insecurity subconstructs based on the 10-item Child Food Insecurity Experiences Scale was estimated. Weighted multinomial logistic regression assessed associations between sociodemographic characteristics and food insecurity experiences as a four-level (no, few, several, or many experiences) variable. Results: Across 2019-2021 among adolescents, the prevalence of worrying about food scarcity ranged between 18.4%-22.5%, worrying about parental/guardian ability to get food ranged between 22.8%-26.9%, and not being able to get the food they wanted ranged between 23.5%-26.1%. Close to or above one in four adolescents affirmed the uncertainty (range: 26.9%-29.9%) and compromised diet quality or preferences (range: 23.5%-26.1%) subconstructs. In 2021, adolescents identifying as Black had a higher relative risk ratio of few food insecurity experiences (adjusted relative risk ratio (ARRR): 2.04 [95% CI: 1.20, 3.47], p-value: <0.01) and adolescents identifying as Indigenous had a higher relative risk ratio of several food insecurity experiences (2.38 [1.10, 5.15], p-value 0.03) compared to adolescents identifying as White. The relative risk ratio of having few, several, or many food insecurity experiences also differed by age, sex-at-birth, perceived income adequacy, and region. Conclusion: The type and number of experiences reported underscores the value of directly measuring food insecurity. Interventions to mitigate food insecurity's adverse consequences are warranted.

BackgroundAdherence to UK dietary guidelines is poor, yet no evidence exists regarding population-level knowledge of these guidelines, or the barriers and facilitators to adherence. This study aimed to characterise knowledge of UK dietary guidelines and perceived barriers and facilitators to adherence in a nationally representative UK sample. MethodsA cross-sectional survey was administered to 1003 adults recruited via Prolific, matched to the UK population by age, sex, and ethnicity. A 22-item knowledge questionnaire assessed awareness of the Eatwell Guide and broader Dietary Reference Values (DRVs), with both strict and liberal scoring applied. Perceived barriers and facilitators to adherence were assessed using custom questionnaire items informed by the COM-B model and TDF framework. ResultsKnowledge of Eatwell Guide recommendations was moderate under strict scoring (53.3%) and improved under liberal scoring (72.5%), despite nearly half of participants reporting no familiarity with the Eatwell Guide. Knowledge of broader DRVs was poor using strict scoring (17.9%) but moderate with liberal scoring (58.9%). The most commonly reported barriers were social (e.g. celebrations), environmental (e.g. access to unhealthy foods), and psychological (e.g., mood). The most strongly endorsed facilitators were economic (e.g. cheaper healthy foods) and health-related (e.g. motivated by weight and mental health). ConclusionsThese findings suggest that whilst knowledge of UK dietary guidelines is reasonable, individualised behaviour change approaches alone are unlikely to be sufficient. Meaningful population-level improvements will require complementary structural changes to the food environment.

Objective: Breast milk is the optimal source of nutrition for preterm infants, however, low breast milk production is common following a preterm birth. This study aimed to determine if taking brewers yeast' or beta-glucan improves daily expressed breast milk volume. Design: Randomised, blinded, parallel, placebo-controlled trial. Setting: Three Australian tertiary level neonatal units. Patients: Mothers with a singleton or twin pregnancy who gave birth at less than 34 weeks' gestation. Interventions: Mothers were randomised within 72 hours of birth into three parallel groups in 1:1:1 ratio to receive either brewers' yeast, beta-glucan or placebo capsules for seven days. Main outcome measure: Total expressed breast milk volume over a 24-hour period on day seven of intervention. Results: A total of 105 mothers underwent randomisation between August 2022 and April 2024 (36 brewers' yeast, 35 beta-glucan, and 34 placebo). The adjusted mean difference in daily expressed breast milk volume was 94 mL/day (95% CI -51 to 239 mL/day) between the brewers' yeast and placebo groups, and -25 mL/day (95% CI -173 to 123 mL/day) between the beta-glucan and placebo groups. Maternal side effects were similar across groups. Conclusion: We found no clear effect of short-term administration of brewers' yeast or beta-glucan on breast-milk production following preterm birth; both interventions were well tolerated. Given the small sample size, these findings do not rule out the possibility of a clinically meaningful benefit of brewers' yeast and suggest further research with a larger sample size may be warranted to clarify the potential clinical impact. Trial registration number ACTRN12622000968774.

Ultra-processed food (UPF) may contribute to increased energy intake and weight gain, but evidence synthesis from randomised controlled trials (RCT) is lacking. A pre-registered systematic review and meta-analysis of RCTs was conducted comparing UPF with less processed food (LPF) on energy intake and/or body weight in humans. Secondary analyses (meta-regression and sub-group) examined effects of UPF on appetite sensations, eating rate, palatability and considered the role of nutrient profile in explaining results. Ten eligible studies were included. UPF trial arms tended to have higher energy intake (standardised mean differences [SMDs]=0.18-0.44), but statistical significance varied between analytic models. Weight gain (SMD=0.65) and eating rate (SMD=0.96) were significantly greater in UPF trial arms. No significant differences in palatability, appetite sensations or energy intake later in the day were observed. Diets (UPF vs. LPF) used in trials were not matched for nutrient profile. Effects on energy intake varied if UPFs were higher (SMD=0.71) or similar (SMD=0.02) in energy density. Current RCTs are suggestive that UPFs may increase energy intake and body weight; however, results may be explained by energy density of foods used. Further research is needed to understand whether the level of processing impacts health outcomes independent to nutrient profile.

Objective: ADHD has been associated with obesity indicators, including BMI, across the lifespan. A possible mechanism linking ADHD and BMI is binge eating. Previous research has found associations between ADHD, binge eating and BMI. However, the role of genetic and environmental influences on these associations remains unclear. Method: We utilized data from the Twins Early Development Study (TEDS), comprising 3,675 monozygotic and 7,063 dizygotic twin pairs. ADHD symptoms in childhood and adolescence were assessed using parent-reported questionnaires. Adult ADHD symptoms were measured using both self-report and parent-report questionnaires. Phenotypic mediation models examined whether binge eating mediated the association between ADHD and BMI, without controlling for genetic confounding. Subsequently, the etiological architecture underlying the associations among the three traits across childhood, adolescence, and adulthood were investigated by incorporating genetic and environmental influences into the models. Results: Binge eating significantly mediated the association between ADHD symptoms and BMI in both adolescence and adulthood. However, these mediation effects were no longer present once genetic and environmental influences were incorporated into the models. The best-fitting model in childhood, adolescence and adulthood was Cholesky decomposition models, where covariance between traits was explained by shared aetiology. Conclusions: This twin study reveals shared liability across ADHD, binge eating, and BMI. The mediating role of binge eating in the relationship between ADHD symptoms and BMI was largely confounded by shared genetic influences. Intervention strategies could focus more on common underlying behavioural and self-regulatory mechanisms across these traits, as well as placing more emphasis on symptom patterns within families.