Appetite

ObjectiveTo characterise the role of Sucrase-isomaltase (SI) in regulating dietary behaviours, such as sweet preference and food liking in Si knockout (Sis-KO) mice and in population-based cohorts from Greenland and the UK. DesignWe profiled the appetitive and post-ingestive response to dietary carbohydrates in SI knockout (Sis-KO) mice. Alongside this, we conducted detailed dietary analysis of 45 foods in two Greenlandic population-based cohorts (IHIT, n=2778 and 68 foods, and B2018, n=2203 and 45 foods) with the presence of a common (allele frequency = 14.3%) SI Loss of function (LoF) variant, c.273-274delAG. Finally, we explored the association between SI hypomorphic variants, liking of 140 foods, and sucrose content using data from 134,766 UKBB participants with exome sequencing and questionnaire data available. ResultsSucrose naive Sis-KO mice had a significantly reduced intake of dietary sucrose, and preference for 10% liquid sucrose, in two-bottle preference studies. Mechanistically, oral administration of the short-chain fatty acid acetate reduced sucrose-preference in wild-type mice. In Greenlandic LoF homozygous carriers we show that the previously reported reduction in sugar intake may primarily be explained by a lower intake of cake and pastries, and of candy and chocolate and that added sugar is the main factor explaining these associations. In the UKBB, a negative association with "cake icing", the food with the highest sucrose content per 100g, was detected in SI hypomorphic carriers, as well as in sensitivity analyses conducted only including carriers of known CSID LoF variants. Further, a negative linear relationship was also observed between the effect estimates of hypomorphic SI variants on food liking and the estimated sucrose content per 100g of 88 sucrose-containing foods, indicating that food dislike in SI carriers correlates with the amount of sucrose in food. ConclusionCollectively, we demonstrated that genetic variation in the SI gene is associated with significant changes in sucrose preference, characterised by a rapid avoidance of dietary sucrose in Sis-KO mice, as well as lower consumption and increased disliking of sucrose rich foods in Greenlanders and Europeans, respectively. This work demonstrates that genetic variation in the SI gene may impact physiology beyond the gastrointestinal tract and suggest the possibility to target SI to reduce the preference, and intake, of dietary sucrose with implications for digestive and metabolic health.

BackgroundAttentional bias (AB) for palatable foods has been linked to overeating, yet data on its modulation with body-mass index (BMI) and hunger/satiety are inconsistent. We tested whether hunger, sensory-specific satiety and BMI interact to shape automatic capture of attention by real high-calorie snack foods. MethodsTwo emotional-attentional-blink (EAB) experiments presented food distractors either 300 msec (lag-3) or 900 msec (lag-9) before a neutral target. Experiment 1 (N = 183; whole BMI range) randomly assigned participants to taste (non-satiated), satiated or non-eating conditions; the snacks eaten (or not eaten) subsequently re-appeared as distractors in the EAB task. Experiment 2 (N = 61; 31 overweight/obese, 30 normal-weight) manipulated hunger/satiety states and snack type (consumed vs. novel) orthogonally, in a double session design. ResultsExperiment 1-- food images presented at lag-3 reduced target detection compared with lag-9 (OR = 0.61, CI 0.50-0.75, p <.01. Higher BMI predicted a larger AB when hungry, but a smaller AB when satiated (OR = 0.65, CI 0.48-0.88, p < 0.01). Experiment 2-- For novel snacks, an interaction revealed that participants with overweight/obesity retained robust AB after satiation, whereas AB declined for participants with normal-weight (OR = 2.45, CI 1.09-5.51, p = 0.03). For snacks just eaten, AB remained significant in both groups (lag-3 vs. lag-9: OR = 0.37, CI 0.25-0.55, p <.001). ConclusionsReal-food cues automatically biased attention regardless of metabolic state, with BMI modulating this effect: even when satiated, individuals with overweight/obesity continue to orient their attention toward both familiar and novel high-calorie foods. These findings suggest that satiety signals alone may be insufficient to curb attentional capture by food in obesity, highlighting the need for interventions that target attentional control and limit food availability.

Bioenergetic failure caused by impaired utilisation of glucose and fatty acids contributes to organ dysfunction across multiple tissues in critical illness. Ketone bodies may form an alternative substrate source, but the feasibility and safety of inducing a ketogenic state in physiologically unstable patients is not known. Twenty-nine mechanically ventilated adults with multi-organ failure were randomised into a two-centre safety and feasibility trial of ketogenic versus standard enteral feeding. Ketogenic feeding was feasible, safe, well tolerated and resulted in ketosis. Patients receiving ketogenic feeding had fewer hypoglycaemic events (0% vs. 1.58%), required less exogenous insulin (0.0 IU (IQR 0-16) vs.78 IU (IQR 0-412) but had slightly more daily episodes of diarrhoea (53.5% vs. 42.9%) over the trial period. Untargeted metabophenotyping revealed altered Cahill cycle flux and bioenergetic states, suggesting an advantageous metabolic profile. Ketogenic feeding is feasible and may be a novel intervention for addressing bioenergetic failure in critically ill patients. Clinical Trials.gov registration: NCT04101071; 19.09.2019. Take-home MessageCritical illness leads to altered metabolic states and bioenergetic failure caused by impaired utilisation of glucose, fatty acids and amino acids. This contributes to organ dysfunction across multiple tissues. Ketones may provide a safe and acceptable alternative metabolic fuel enabling energy production and maintaining tissue homeostasis. TweetKetogenic enteral feeding in early critical illness is feasible, safe and may decrease insulin requirements.

ObjectivesRestricting fermentable oligosaccharides, disaccharides, monosaccharides, and polyols (FODMAPs) intake can alleviate symptoms in children with gut-brain interaction disorders (DGBI). Due to the restrictive nature of the low FODMAP diet (LFD), the less restrictive FODMAP Gentle diet (FGD) has been suggested. However, the types of high FODMAP foods and carbohydrates commonly consumed by US children are unknown, as is the impact of the FGD on a typical diet. This project aimed to identify the high FODMAP foods and proportions of FODMAP carbohydrates consumed by children with DGBI and healthy children (HC), and to determine which usually ingested FODMAPs would be restricted on the FGD. MethodsThree-day diet records from both HC and children with DGBI were analyzed to assess the type of high FODMAP foods and carbohydrates ingested. Results were compared between the groups. The ingested FODMAPs that would be restricted on the FGD was determined. ResultsThe number of foods ingested daily was similar between children with DGBI and HC (12.3 {+/-} 4.2 vs 12.9 {+/-} 3.4, respectively); high FODMAP foods comprised most foods eaten in both groups. Children with DGBI (vs HC) ate less high FODMAP foods per day (6.5 {+/-} 2.3 vs 8.7 {+/-} 2.4, P<0.0001, respectively). Fructans were the most consumed FODMAP carbohydrate in both groups and children with DGBI (vs HC) consumed fewer fructans, lactose, fructose, and polyols (all P<0.0001). The top 3 food categories consumed in both groups were wheat-containing foods, dairy, and fruits and 100% fruit juices. In children with DGBI, 80.9% of the high FODMAP foods consumed would be limited on the FGD. DiscussionChildren with DGBI consume significantly fewer high FODMAP foods and carbohydrates than HC. In both groups, the top consumed FODMAP carbohydrates are fructans, lactose, and fructose. A FODMAP Gentle diet would restrict a large majority of high FODMAP foods consumed by children with DGBI.

ObjectiveThe Nine Item ARFID Screen (NIAS) is a widely used measure assessing symptoms of avoidant/restrictive food intake disorder (ARFID). Previous studies suggest that individuals with eating disorders driven by shape/weight concerns also have elevated scores on the NIAS. To further clarify this issue, we characterized NIAS scores in a large sample of individuals with eating disorders and evaluated overlap in symptoms measured by the NIAS and the Eating Disorder Examination-Questionnaire (EDE-Q) version 6.0. MethodOur sample comprised 9,148 participants from the Eating Disorders Genetics Initiative Sweden (EDGI-SE), who completed surveys including NIAS and EDE-Q. NIAS scores were calculated and compared by eating disorder diagnostic group using descriptive statistics and linear models. ResultsParticipants with current anorexia nervosa demonstrated the highest mean NIAS scores and had the greatest proportion (57.0%) of individuals scoring above a clinical cutoff on at least one of the NIAS subscales. Individuals with bulimia nervosa, binge-eating disorder, and other specified feeding or eating disorder also demonstrated elevated NIAS scores compared to individuals with no lifetime history of an eating disorder (ps < .05). All subscales of the NIAS showed small to moderate correlations with all subscales of the EDE-Q (rs = 0.26-0.40). DiscussionOur results substantiate that individuals with eating disorders other than ARFID demonstrate elevated scores on the NIAS, suggesting that this tool is inadequate on its own for differentiating ARFID from shape/weight-motivated eating disorders. Further research is needed to inform clinical interventions addressing the co-occurrence of ARFID-related drivers and shape/weight-related motivation for dietary restriction.

BackgroundEarly temperament may shape childrens eating behaviours and growth, yet longitudinal evidence supporting these associations remains limited. We aimed to identify latent temperament profiles from 6 months to 5 years and examine their associations with eating behaviours and longitudinal changes in BMI-SDS. MethodsData were drawn from the FinnBrain Birth Cohort Study, a population based longitudinal study in Southwest Finland (n=2,286). Child temperament was assessed at 6 and 12 months, and at 2, 4, and 5 years using validated questionnaires. Eating behaviour was reported at age 2, and BMI-SDS was measured at ages 2 and 5. Latent profile analysis was conducted on repeated temperament measures. Associations with outcomes were examined using the BCH method. ResultsThree temperament profiles emerged: Dysregulated group (38%; low self-regulation, low to average positive reactivity, low negative reactivity), High self-regulation group (37%: high self-regulation, low negative reactivity, high to average positive reactivity), High negative reactivity group (24%: high negative reactivity, moderate positive reactivity, average self-regulation). The high self-regulation group showed more favorable eating behaviours (less snacking and fussiness, more willingness to taste new foods) compared to the other groups. High negative reactivity group showed greater decrease in BMI than Dysregulated group. Other BMI change differences were non-significant. ConclusionsDistinct temperament profiles were linked to early eating behaviours and, to a lesser extent, BMI development. Understanding these early temperament-based patterns may help identify children at risk for less favourable eating patterns and inform tailored early interventions to promote healthy eating and growth.

BackgroundDistracted eating is prevalent in modern environments. While behavioral research consistently shows that distraction attenuates taste perception and increases food intake, the underlying neural mechanisms appear to be more complex. ObjectiveThis functional magnetic resonance imaging (fMRI) study investigated whether naturalistic distraction modulates gustatory processing via sensory suppression or reallocation of neural resources, as observed in more controlled cognitive load paradigms. MethodsThirty-eight healthy participants received sweet and umami taste stimuli of low and high concentration during fMRI scanning. Attentional state was manipulated using short food-related (low-distraction) versus film-related (high-distraction) video clips. After each video, participants rated perceived intensity and pleasantness. Group-level analyses included covariates for sex, body mass index (BMI), and hunger level. ResultsHigh distraction attenuated perceived intensity (p < 0.001, d = -0.28) and pleasantness (p < 0.01, d = -0.21), independent of taste category or concentration. No significant attenuation by distraction was observed in core gustatory regions (insula, orbitofrontal cortex). Instead, distraction increased activation in occipital, thalamic, and cerebellar regions, indicating a redistribution of processing resources toward visual and attentional systems. ConclusionDistraction reduced taste salience without lowering gustatory cortex activity, supporting resource-competition models rather than active sensory suppression. These results reinforce that the impact of distracted eating is behaviorally robust yet neurally subtle, highlighting the need for personalized stimuli and ecologically valid methods to capture real-world eating behavior. The study demonstrates that video-based paradigms work reliably in fMRI and capture how naturalistic distraction alters taste experience.

BackgroundDespite its common early onset, little is known about the prevalence and clinical presentation of avoidant restrictive food intake disorder (ARFID) in very young children, hindering early identification and intervention. Differentiating ARFID from normative selective eating is particularly challenging, yet validated parent-reported screening tools are lacking. This study aimed to estimate the point prevalence and describe the clinical characteristics of ARFID in preschoolers. It also evaluated the psychometric properties of the parent-reported ARFID-Brief Screener by assessing its agreement with a diagnostic interview for ARFID. MethodsParents of 645 children (50.5% male, mean age 3.2 years) completed the ARFID-Brief Screener and a neurodevelopmental screener during 2.5- and 4-year routine check-ups at 21 child health centers in West Sweden. Parents of all screen-positive and of randomly selected screen-negative children were invited to a follow-up diagnostic interview via phone. Additional clinical data were extracted from health records. ResultsOf the 42 children (6.5%) who screened positive for ARFID, 29 were followed up via diagnostic interview, and 21 received an ARFID diagnosis, yielding a positive predictive value of 72%. Negative predictive value, sensitivity, specificity, and overall accuracy of the ARFID-Brief Screener were 94%, 91%, 79%, and 84%, respectively. The estimated point prevalence of ARFID was 5.9%. All diagnosed children exhibited both sensory-based avoidance and low interest in eating. Only 13.5% met ARFID criteria based on weight- or nutrition-related impairment (DSM-5 Criteria A1-A3). Two fifths (39.1%) of children with ARFID exhibited early language delays compared to 13.5% of children without ARFID. More extensive neurodevelopmental problems were associated with greater ARFID severity and with higher scores on the sensory and concern profiles. ConclusionsARFID is not uncommon among preschoolers, though prevalence may be slightly overestimated in this study. It is primarily characterized by sensory-based avoidance and low interest in eating, and by psychosocial impairment instead of physical health consequences, underscoring the need to assess impact beyond weight, growth, and nutrition. Early neurodevelopmental difficulties are overrepresented, highlighting their relevance for early detection and intervention. The ARFID-Brief Screener demonstrated promising psychometric properties and may be a valuable tool for routine screening, though follow-up assessments remain necessary to confirm a diagnoses. Plain English summaryAvoidant restrictive food intake disorder (ARFID) often starts early in life, but little is known about how common it is in very young children. This study looked at how many preschool-aged children have ARFID and what their eating difficulties look like. We also tested how well a short parent questionnaire, the ARFID-Brief Screener, can help identify children at risk. Parents of 645 Swedish children filled out the screener during routine health check-ups at age 2.5 or 5. Children who screened positive and a randomly selected group of screen-negative children were invited to a follow-up interview. Based on these interviews, we estimated that about 5.9% of preschoolers may have ARFID. All children with ARFID avoided food due to sensory sensitivities or had little interest in eating. Few had weight or nutrition problems, but many experienced difficulties in daily life, such as stressful mealtimes. Children with ARFID were more likely to have early neurodevelopmental challenges such as delayed language development, suggesting that these symptoms may aid in identifying children at risk for ARFID. The ARFID-Brief Screener performed well in detecting at-risk children, but follow-up assessments are still needed to confirm a diagnosis.

Background Emerging evidence highlights the gut-brain axis as a key pathway linking diet and anxiety, yet the key determinants remain unclear. Most studies have focused on single components of diet and rarely integrate long- and short-term intake. Furthermore, prior gut-brain work has focused on microbiome composition, while functional features remain underexplored. In this study, we investigated associations between long- and short-term dietary intake, gut microbiome composition and functions, and anxiety in a subclinical cohort of 46 females (18-24 years) from the United Kingdom. Results Long-term diet quality was assessed using the Healthy Eating Index (HEI-2020) derived from a food frequency questionnaire, stratifying participants into lower and higher diet quality clusters. Short-term dietary intake was assessed via 24-hour recalls. Shotgun metagenomics of stool samples was used to assess differences in alpha and beta diversity indices, species abundances, and bacterial pathways putatively metabolizing gut-brain-axis-relevant molecules. Anxiety was measured using the State-Trait Anxiety Inventory (state subscale STAI-s). Regression models identified diet quality (HEI cluster) as the primary dietary feature of anxiety variation. The presence of Ruminococcus gnavus and Flavonifractor plautii and the abundances of Bilophila wadsworthia and Bacteroides thetaiotaomicron were positively associated with anxiety. The presence of Feacalibacterium prausnitzii and greater abundances of butyrate, propionate, and GABA synthesis pathways were inversely associated with anxiety. Non-linear models revealed a U-shaped relationship between inositol synthesis and STAI-s. Finally, we found that habitual diet quality may modulate anxiety-related responses to short-term dietary variation. Conclusions These findings reveal widespread links between long-term diet quality, microbiota composition and function, and anxiety symptoms. These results point towards several promising targets for prebiotic, probiotic, postbiotic, and dietary interventions aimed at reducing anxiety.

Orthorexia involves an obsessive tendency towards "healthy" foods. It is a risk factor for eating disorders (anorexia nervosa and the proposed "orthorexia nervosa") and psychological distress, but its biological mechanism remains unknown. We hypothesised that this mechanism operates through the stomach: increased gastric power differentiates appetising from unappetising foods, vagal stimulation reduces food liking, and gastric proto-nausea can be evoked by disgust; all contributors to disordered eating. We used electrogastrography alongside high-density facial landmark tracking to gauge responses to minimally processed ("healthy"), highly processed ("unhealthy"), and culturally unaccepted ("disgusting") foods in a non-clinical sample (N=77). Trait orthorexia was associated with increased self-reported desire to eat healthy foods. Moreover, we found that higher orthorexia was associated with increasing disgust-related facial responses to unhealthy and disgusting foods. We then identified a relationship between food-healthiness ratings and gastric power: those who generally assigned lower healthiness ratings to foods showed higher gastric power for unhealthy than healthy foods, whereas those who expressed higher healthiness ratings showed higher gastric power for healthy over unhealthy foods. This suggests that the stomach tracks individual differences in eating preferences. Crucially, and contrary to our expectations, higher trait orthorexia was associated with a paradoxical increase in gastric power to unhealthy foods. One explanation is that higher gastric power for unhealthy foods reflects increased appetite for self-denied foods. Alternatively, orthorexia itself could be an adaptive response to exert stronger cognitive control over a pre-existing gastric appetite for unhealthy foods.

Clinical practice guidelines for medical professionals working with children and adolescents recommend routine screening for eating disorders. However, no validated screening tools exist for this age group. The aim of this study was to design and validate a brief, caregiver-based screening tool for eating disorders in children ages 6-12 that can be used in primary care. Caregivers of children aged 6-12 completed a battery of questionnaires (N=1,760). A subsample of caregivers completed semi-structured diagnostic interviews (n=255) to evaluate child eating disorder diagnosis. Standard data science practices were used to determine which questions were best at detecting an eating disorder and the most appropriate scoring threshold. Our final screener consists of two items that were effective at discriminating between children with an eating disorder and those without one and that were general enough to capture multiple diagnoses. As is recommended by organizations such as the AAP, this tool would ideally be administered to all caregivers of children ages 6-12 at yearly wellness visits beginning at the age of 6.

ObjectiveA growing literature suggests manipulating dietary protein status decreases sweet consumption in rodents and in humans. Underlying neurocircuit mechanisms have not yet been determined, but previous work points towards hedonic rather than homeostatic pathways. Here we hypothesized that a history of protein restriction reduces sucrose seeking by altering mesolimbic dopamine signaling. MethodsWe tested this hypothesis using established behavioral tests of palatability and motivation, including the palatability contrast and conditioned place preference (CPP) tests. We used modern optical sensors for measuring real-time nucleus accumbens (NAc) dopamine dynamics during sucrose consumption, via fiber photometry, in male C57/Bl6J mice maintained on low-protein high-carbohydrate (LPHC) or control (CON) diet for [~]5 weeks. ResultsA history of protein restriction decreased the consumption of a sucrose dessert in sated mice by [~]50% compared to controls [T-test, p< 0.05]. The dopamine release in NAc during sucrose consumption was reduced, also by [~]50%, in LPHC-fed mice compared to CON [T-test, p< 0.01]. Furthermore, LPHC-feeding blocked the sucrose-conditioned place preference we observed in CON-fed mice [paired T-test, p< 0.05], indicating reduced motivation. This was accompanied by a 33% decrease in neuronal activation of the NAc core, as measured by c-Fos immunolabeling from brains collected directly after the CPP test. ConclusionsDespite ongoing efforts to promote healthier dietary habits, adherence to recommendations aimed at reducing the intake of added sugars and processed sweets remains challenging. This study highlights chronic dietary protein restriction as a nutritional intervention that suppresses the motivation for sucrose intake, via blunted sucrose-evoke dopamine release in NAc.

Obesity is a growing public health concern with more than 40% of adults meeting criteria for obesity in the United States. Although many treatments seek to lower individuals weight, few treatments have focused on cognitive strategies to change the way individuals think about food, therefore, decreasing consumption of non-nutrient-dense foods. Cognitive reappraisal is one strategy that involves changing the way one thinks about a situation and can be used to downregulate responses to those stimuli. Leveraging this intuitive, cost-effective strategy to decrease ones desire to eat unhealthy food and therefore, decrease overeating, could improve physical and mental health. The present study identified brain regions that are differentially activated when using cognitive reappraisal to downregulate responses to food (FR) versus when using the same strategy to downregulate negative emotions (ER). We collected functional magnetic resonance imaging (fMRI) data in 63 undergraduate students while participants completed both tasks. There was increased reappraisal-related activation in widespread regions across both tasks, including in expected subcortical (i.e., striatum) and cortical areas (i.e., visual, frontoparietal). We also found domain-specific activity, with greater insula activation in the FR than the ER task and greater hippocampal activation in the ER than the FR task. These results reveal domain-general and domain-specific effects of cognitive reappraisal in FR and ER tasks that inform future work examining eating behavior. Taken together, a better explication of the overlapping and discrete processes of food regulation, as it compares to other applications of this regulatory strategy can inform new intervention targets.

Maladaptive exercise (MalE) includes excessive, compulsive, or compensatory exercise and is a common eating-disorder (ED) symptom associated with increased severity, slower rates-of-recovery, and faster rates-of-relapse. Affect-regulation theories posit that MalE functions to reduce high negative affect (NA), although support for the affect-regulation model is mixed. Previous studies have not integrated ecological momentary assessment (EMA) with accelerometry or examined the affect-regulation model in individuals with EDs who frequently engage in MalE. The objective of this study was to examine trajectories of NA and positive affect (PA) through a 7-day EMA study combined with wrist-worn accelerometry in women with EDs (N=84). Piecewise generalized mixed-effects regression models evaluated the trajectories of PA and NA in the hours leading up to and following self-reported exercise and exercise identified via accelerometry. NA was increasing before self-reported exercise, although NA did not meaningfully change relative to objectively measured exercise. PA was increasing prior to exercise and decreasing after exercise, and this pattern was consistent for both self-reported and objectively measured exercise. Rates of rising PA were steeper in the hours leading up to higher intensity exercise episodes. Though inconsistent with affect-regulation models, the current study offers preliminary evidence that exercise is associated with disrupted affective responses among women with EDs who regularly engage in MalE. Results suggest that planning or anticipating high-intensity exercise may be rewarding for a considerable proportion of people with EDs. If replicated, treatments may consider decreasing the reward value placed on intense exercise and increasing value placed on low-intensity or non-exercise activities.

Background & AimsAlternating periods of excessive and restrained eating results in weight cycling, a known risk factor for eating behavior dysregulation such as binge eating. Diet alternation also induces changes in intestinal microbiota composition. We tested the hypothesis that recurrent diet alternation alters hedonic feeding regulation by changing either or both intestinal microbiota and brain homeostasis in mouse. MethodsC57BL/6 mice underwent 3 cycles of 1 week of western diet (WD, 45% kcal from fat) separated by 2 weeks of chow diet (CYCL group) or staid under chow diet (CTRL group). Food intake was monitored after each dietary change. Striatum, hypothalamus, brainstem and caecal content were collected before the third WD introduction in CYCL mice and in CTRL mice. Microbiota transfer from CYCL or CTRL mice into naive recipient mice was performed to investigate whether gut microbiota per se could explain differences in eating behavior during weight cycling. ResultsDiet alternation in CYCL mice resulted in weight cycling, with enhanced weight gain upon each WD feeding phase. CYCL mice increased their energy intake specifically during the first hours following WD re-introduction, reminiscent of binge-eating episodes. Expression of reward-related genes in the striatum and thickness of the astro-glial barrier in the brain stem were enhanced in CYCL compared to CTRL mice. Diet alternation also induced caecal dysbiosis in CYCL mice. Gut microbiota transfer from CYCL mice to naive recipient mice recapitulated the altered eating behavior upon WD exposure. ConclusionsAlternation between high-energy and standard diet durably remodels the gut microbiota and the brain towards a profile associated with an increase in hedonic appetite. Using gut microbiota transfer, we established that this microbiota signature affects hedonic feeding regulation. These results open the ways to microbiota-targeted strategies to prevent development of eating disorders in weight cycling patients.

ObjectiveThe current study investigated whether dietary restraint moderates the relationship between Postprandial Distress Syndrome (PDS) symptoms (e.g., postprandial fullness, early satiety, and nausea) and Binge Eating (BE) in adolescents with overweight and obesity. BE is associated with PDS symptoms. Individuals often self-initiate restrictive diets that limit food variety in attempt to manage PDS symptoms. However, dietary restraint is thought to increase frequency of BE. Thus, individuals who attempt to manage PDS symptoms through dietary restraint may engage in more BE. Investigating the relationship between dietary restraint and PDS in relation to BE will increase our understanding of risk factors for BE during adolescence--a period associated with heightened onset of disordered eating and dieting attempts. MethodAdolescents (N=60) with higher weight (M Body Mass Index (BMI) percentile = 97.72 [SD = 2.61], M age = 15.37 years [SD = 1.34], 63.3% female) completed measures of PDS symptoms, dietary restraint, and BE. Generalized linear regression examined whether dietary restraint moderated the relationship between PDS symptoms and BE frequency. ResultsThe interaction effect was significant, such that greater PDS symptoms were associated with increased BE frequency when dietary restraint was average or higher than average. DiscussionResults suggest that the relationship between PDS and BE symptoms depends on level of dietary restraint. Future work should investigate if this relationship holds for other GI syndromes and investigate the differential impact of dietary restraint versus restriction on PDS and BE.

How much pleasure we take in eating is more than just how much we enjoy the taste of food. Food involvement - the amount of time we spend on food beyond the immediate act of eating and tasting - is key to the human food experience. We took a biological approach to test whether food-related behaviors, together capturing food involvement, have genetic components and are partly due to inherited variation. We collected data via an internet survey from a genetically informative sample of 419 adult twins (114 monozygotic twin pairs, 31 dizygotic twin pairs, and 129 singletons). Because we conducted this research during the pandemic, we also ascertained how many participants had experienced COVID-19-associated loss of taste and smell. Since these respondents had previously participated in research in person, we measured their level of engagement to evaluate the quality of their online responses. Additive genetics explained 16-44% of the variation in some measures of food involvement, most prominently various aspects of cooking, suggesting some features of the human food experience may be inborn. Other features reflected shared (early) environment, captured by respondents twin status. About 6% of participants had a history of COVID-19 infection, many with transitory taste and smell loss, but all but one had recovered before the survey. Overall, these results suggest that people may have inborn as well as learned variations in their involvement with food. We also learned to adapt to research during a pandemic by considering COVID-19 status and measuring engagement in online studies of human eating behavior.

Vagus nerve signals from the gut to brain carry information about nutrients and drive food reward. Such signals are disrupted by consuming large amounts of high-calorie foods, necessitating greater food intake to elicit a similar neural response. Non-invasive vagus nerve stimulation (nVNS) via a branch innervating the ear is a candidate treatment for obesity in humans. There is disagreement on the optimal location of nVNS in the ear for experimental and clinical studies. There are also no studies comparing nVNS in hungry and full states. We aimed to compare ear position(s) for nVNS and explore the effects of nVNS during hungry and full states on proxies for autonomic outflow (heart-rate variability) and efferent metabolism (gastric frequency and resting energy expenditure). In a within-subject design, 14 participants (10 women, on average 29.4 +/- 6.7 years old) received nVNS in four different locations (cymba conchae, tragus, earlobe, or tragus AND cymba conchae) on separate days. In each session, participants were asked to consume a palatable chocolate flavored milk. With electrography on the abdomen and indirect calorimetry in a canopy, we measured electro-cardiogram, electro-gastrogram and resting energy expenditure for 15 minutes before and at least 35 minutes after consumption of the palatable drink. We also collected ratings of the palatable drink and internal and other states. Pre-drink consumption (in a hungry state) we observed no differences in the effect of location of acute nVNS on resting energy expenditure and gastric frequency. However, nVNS in cymba conchae decreases heart-rate variability and ratings of how much participants want to consume the drink. After drink consumption and with continued nVNS, gastric frequency is unchanged, and resting energy expenditure increases regardless of stimulation location. Heart-rate variability decreases in all locations, except cymba conchae. We also observe a trend for an increase in gastric frequency in late post-drink consumption time-points in cymba conchae. These results suggest that nVNS in the cymba conchae in a hungry state has a similar acute effect on vagal tone as food consumption: to decrease heart rate variability. This effect then negates the usual postprandial effects of a decrease in heart rate variability as seen in the other nVNS locations. This suggests that nVNS in cymba conchae may act primarily on vagal afferent autonomic (and only modestly on metabolic output) in a similar way as food consumption does. HighlightsO_LIWe measured autonomic outflow and efferent metabolism before and after consumption C_LIO_LIWe manipulated the location of nVNS stimulation in the outer ear C_LIO_LIThe different locations were earlobe, cymba conchae, tragus, cymba conchae+tragus C_LIO_LInVNS in cymba conchae decreases pre-consumption heart-rate variability and wanting C_LIO_LInVNS in other locations decreases post-consumption heart-rate variabilty C_LI

BackgroundPrebiotic dietary fiber and related metabolites have been suggested to attenuate low-grade systemic and central inflammation through improving gut-brain axis signaling. We here aimed to test whether habitual or short-term high-dose fiber intake is linked to inflammatory markers in blood and to indicators of central hypothalamic inflammation. MethodsIn total, 59 adults (19 women, aged 28.3 years {+/-} 6.6 SD, mean body mass index, BMI, 27.3 {+/-} 1.5 SD) were included into analyses. Participants completed a food frequency questionnaire, underwent diffusion-weighted magnetic resonance imaging (MRI) at 3 Tesla for provision of mean diffusivity (MD) as a marker of brain tissue inflammation and donated fasting blood. Measurements took place at up to 4 timepoints, i.e. before and after 14 days of supplementary fiber and placebo intake, respectively. High-sensitive C-reactive protein (CRP), tumor-necrosis factor alpha (TNF-) and interleukin-6 (IL6) were assessed in serum. The study was preregistered at https://osf.io/uzbav. ResultsHabitual and interventional high-fiber diet was not significantly associated with neither inflammatory markers (|{beta}intervention|> 0.1, p > 0.32) nor with hypothalamic MD (|{beta}intervention| = 1.8, p = 0.07) according to linear mixed effects modeling. Male sex and higher body fat mass related to higher CRP. Further, higher BMI was borderline related to lower hypothalamic MD. ConclusionsIn this sample of overweight adults, dietary fiber intake was not related to inflammatory blood markers or hypothalamic microstructure. Instead, sex and body composition were of higher importance for prediction of interindividual differences in markers of (neuro)inflammation. Significance StatementPrebiotic dietary fiber has been discussed to lower systemic and central inflammation. While previous studies investigated the effects of fiber on inflammatory blood markers, the knowledge of the effect of fiber on neuroinflammation is limited. Thus, in this pre-registered randomized controlled trial analysis we examined the relationship between dietary fiber intake and inflammatory markers in blood and hypothalamus. 3T MRI and blood markers were assessed before and after high-fiber intake and placebo in 59 adults. In our overweight study sample of 19-42 years old adults, fiber intake had no significant impact on inflammatory markers. The current null findings can inform future nutrition neuroimaging trials and add to the discussion about how diet may affect brain structure and function.

BackgroundObesogenic diets (ODs) are known to trigger metabolic and inflammatory disturbances. However, the effects of short-term OD withdrawal on systemic and neuroinflammatory parameters remain unclear. ObjectivesThis study investigated the short-term effects of OD withdrawal on metabolic, inflammatory, and anxiety-like behaviours in young male Wistar rats. MethodsThree-week-old male Wistar rats were fed either a control (Ct, n=5) or high-sugar/high-fat (HSHF) diet for 14 days. Animals in the HSHF group were further divided into no-withdrawal (NWt, n=5) and withdrawal (Wt, n=5) groups, where Wt received a control diet for 48 hours. Food intake, body mass, adiposity, serum metabolic parameters, hepatic energy stores, inflammatory markers (serum, liver, hypothalamus, hippocampus, mesenteric fat), and oxidative stress markers in the hippocampus were measured. Anxiety-like behaviour was assessed using the elevated plus maze. ResultsOD intake significantly increased caloric intake, visceral adiposity, hepatic glycogen, and TAG levels. The 48-hour withdrawal reduced TAG, induced hyperinsulinemia and hypoglycaemia, and heightened inflammation in mesenteric fat, serum, and the hippocampus. Oxidative stress markers (SOD and MDA) increased in the hippocampus, correlating with elevated serum corticosterone and heightened anxiety-like behaviour in the Wt group compared to the other groups. ConclusionShort-term withdrawal after only two weeks of OD intake exacerbates systemic and neuroinflammation, hippocampal oxidative stress, and anxiety-like behaviours, indicating rapid negative responses to dietary transition. These findings highlight the metabolic and behavioural challenges associated with short-term OD withdrawal and highlight the need for adjunct interventions to mitigate its adverse effects.