Metabolic sensing in AgRP regulates sucrose preference and dopamine release in the nucleus accumbens.

Hunger increases the motivation for calorie consumption, often at the expense of low-taste appeal. However, the neural mechanisms integrating calorie-sensing with increased motivation for calorie consumption remain unknown. Agouti-related peptide (AgRP) neurons in the arcuate nucleus of the hypothalamus sense hunger, and the ingestion of caloric solutions promotes dopamine release in the absence of sweet taste perception. Therefore, we hypothesised that metabolic-sensing of hunger by AgRP neurons would be essential to promote dopamine release in the nucleus accumbens in response to caloric, but not non-caloric solutions. Moreover, we examined whether metabolic sensing in AgRP neurons affected taste preference for bitter solutions under conditions of energy need. Here we show that impaired metabolic sensing in AgRP neurons attenuated nucleus accumbens dopamine release in response to sucrose, but not saccharin, consumption. Furthermore, metabolic sensing in AgRP neurons was essential to distinguish nucleus accumbens dopamine response to sucrose consumption when compared with saccharin. Under conditions of hunger, metabolic sensing in AgRP neurons increased the preference for sucrose solutions laced with the bitter tastant, quinine, to ensure calorie consumption, whereas mice with impaired metabolic sensing in AgRP neurons maintained a strong aversion to sucrose/quinine solutions despite ongoing hunger. In conclusion, we demonstrate normal metabolic sensing in AgRP neurons drives the preference for calorie consumption, primarily when needed, by engaging dopamine release in the nucleus accumbens.

microRNA-33 controls hunger signaling in hypothalamic AgRP neurons.

AgRP neurons drive hunger, and excessive nutrient intake is the primary driver of obesity and associated metabolic disorders. While many factors impacting central regulation of feeding behavior have been established, the role of microRNAs in this process is poorly understood. Utilizing unique mouse models, we demonstrate that miR-33 plays a critical role in the regulation of AgRP neurons, and that loss of miR-33 leads to increased feeding, obesity, and metabolic dysfunction in mice. These effects include the regulation of multiple miR-33 target genes involved in mitochondrial biogenesis and fatty acid metabolism. Our findings elucidate a key regulatory pathway regulated by a non-coding RNA that impacts hunger by controlling multiple bioenergetic processes associated with the activation of AgRP neurons, providing alternative therapeutic approaches to modulate feeding behavior and associated metabolic diseases.

Differences in dietary acceptability, restraint, disinhibition, and hunger among African American participants randomized to either a vegan or omnivorous soul food diet.

The Nutritious Eating with Soul study was a 24-month, randomized behavioral nutrition intervention among African American adults. This present study, which is a secondary analysis of the NEW Soul study, examined changes in dietary acceptability, restraint, disinhibition, and hunger. Participants (n = 159; 79% female, 74% with ≥ college degree, mean age 48.4 y) were randomized to either a soul food vegan (n = 77) or soul food omnivorous (n = 82) diet and participated in a two-year behavioral nutrition intervention. Questionnaires assessing dietary acceptability (Food Acceptability Questionnaire; FAQ) and dietary restraint, disinhibition, and hunger (Three-Factor Eating Questionnaire; TFEQ) were completed at baseline, 3, 6, 12, and 24 months. Mixed models were specified with main effects (group and time) and interaction effects (group by time) to estimate mean differences in FAQ and TFEQ scores using intent-to-treat analysis. After adjusting for employment, education, food security status, sex, and age, there were no differences in any of the FAQ items, total FAQ score, dietary restraint, disinhibition, and hunger at any timepoint except for one item of the FAQ at 12 months. Participants in the vegan group reported a greater increase in satisfaction after eating a meal than the omnivorous group (mean difference 0.80 ± 0.32, 95% CI 0.18, 1.42; P = 0.01). This is one of the first studies to examine differences in dietary acceptability, hunger, and other eating factors among African American adults randomized to either a vegan or omnivorous soul food diet. The findings highlight that plant-based eating styles are equally acceptable to omnivorous eating patterns and have similar changes in hunger, restraint, and disinhibition. These results suggest that plant-based eating styles can be an acceptable dietary pattern to recommend for cardiovascular disease prevention and may result in greater post-meal satisfaction.

The Calmodulin-interacting peptide Pcp4a regulates feeding state-dependent behavioral choice in zebrafish.

Animals constantly need to judge the valence of an object in their environment: is it potential food or a threat? The brain makes fundamental decisions on the appropriate behavioral strategy by integrating external information from sensory organs and internal signals related to physiological needs. For example, a hungry animal may take more risks than a satiated one when deciding to approach or avoid an object. Using a proteomic profiling approach, we identified the Calmodulin-interacting peptide Pcp4a as a key regulator of foraging-related decisions. Food intake reduced abundance of protein and mRNA of pcp4a via dopamine D2-like receptor-mediated repression of adenylate cyclase. Accordingly, deleting the pcp4a gene made zebrafish larvae more risk averse in a binary decision assay. Strikingly, neurons in the tectum became less responsive to prey-like visual stimuli in pcp4a mutants, thus biasing the behavior toward avoidance. This study pinpoints a molecular mechanism modulating behavioral choice according to internal state.

Post-exercise energy replacement might lead to reduced subsequent energy intake in women with constitutional thinness: Exploratory results from the NUTRILEAN project.

While people with Constitutional Thinness (CT) declare a deep willingness to gain weight, there appetitive responses to energy balance manipulations remain unclear. The present work compares the effect of an acute exercise combined or not with an energy replacement load, on subsequent energy intake, appetite and food reward, between normal weight and women with CT. Anthropometric measurements, body composition (Dual X-ray absorptiometry-DXA) and aerobic capacity (VO2max) were assessed in 10 normal-weight (Body Mass Index-BMI): 20-25 kg/m2) and 10 C T (BMI<17.5 kg/m2) women (18-30 years). They randomly performed i) a resting session (CON); ii) an exercise session (EX); iii) an exercise session with energy replacement (EX + R). Their subsequent ad libitum intake, appetite feelings and food reward were evaluated (Leeds-Food-Preference-Questionnaire). CT showed a lower weight (p < 0,001), BMI(p < 0,001), Fat-Mass (%) (p = 0,003) and Fat-Free Mass (kg) (p < 0,001). CT showed a lower ad libitum energy intake on EX + R compared with CON (p = 0,008) and a higher Relative Energy Intake (REI) on CON compared with EX (p = 0,007) and EX + R (p < 0,001). A lower was observed during EX and EX + R compared with CON (p = 0,006,p = 0,009 respectively) in CT. No condition nor group effect was found for hunger. NW only showed a higher pre-meal fullness on EX + R compared to CON and EX (p < 0,001). Choice (p = 0,030), Explicit Liking (p = 0,016), Explicit Wanting (p = 0,004) and Implicit Wanting (p = 0,035) for taste were higher on EX + R than CON and EX. The decreased EI observed in CT when the exercise-induced energy expenditure is compensated by the ingestion of an equivalent energy load, might contribute to explain the difficulty to increase their energy balance and then induce weight gain. Further studies are needed to better understand their energy balance regulation to propose adapted weight gain strategies.

Human hunger as a memory process.

Hunger refers to (1) the meaning of certain bodily sensations; (2) a mental state of anticipation that food will be good to eat; and (3) an organizing principal, which prioritizes feeding. Definitions (1) and (2) are the focus here, as (3) can be considered their consequent. Definition (1) has been linked to energy-depletion models of hunger, but these are no longer thought viable. Definition (2) has been linked to learning and memory (L&M) models of hunger, but these apply just to palatable foods. Nonetheless, L&M probably forms the basis for hunger generally, as damage to declarative memory can eradicate the experience of hunger. Currently, there is no general L&M model of hunger, little understanding of how physiology intersects with a L&M approach, and no understanding of how Definitions (1) and (2) are related. We present a new L&M model of human hunger. People learn associations between internal (e.g., tummy rumbles) and external cues (e.g., brand names) and food. These associations can be to specific foods (episodic memories) or food-related categories (semantic memories). When a cue is encountered, it may lead to food-related memory retrieval. If retrieval occurs, the memory's affective content allows one to know if food will be good to eat now-hunger-a cognitive operation learned in childhood. These memory processes are acutely inhibited during satiety, and chronically by multiple biological parameters, allowing physiology to modulate hunger. Implications are considered for the process of making hunger judgments, thirst, the cephalic phase response, and motivational and lay theories of hunger. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

GLP-1 response during pregnancy: variations between trimesters and associations with appetite sensations and usual energy intake.

Further research is required to understand hormonal regulation of food intake during pregnancy and its association with energy intake. The objectives are to (i) compare postprandial responses of plasma glucagon-like peptide-1 (GLP-1) between trimesters, (ii) compare postprandial appetite sensations between trimesters, and (iii) examine trimester-specific associations between GLP-1 levels, appetite sensations, and usual energy intake. At each trimester, participants (n = 26) consumed a standard test meal following a 12 h fast. Plasma GLP-1 levels were measured by enzyme-linked immunosorbent assay method at fasting and at 30, 60, 120, and 180 min postprandial. A visual analogue scale assessing appetite sensations was completed at fasting and at 15, 30, 45, 60, 90, 120, 150, and 180 min postprandial. Mean energy intake was assessed using three web-based 24 h dietary recalls at each trimester. Lower postprandial GLP-1 responses were observed in the 2nd (p = 0.004) and 3rd trimesters (p < 0.001) compared to the 1st trimester. Greater postprandial sensations of desire to eat, hunger, and prospective food consumption were noted in the 3rd trimester compared to the 1st trimester (p < 0.04, for all). Fasting GLP-1 was negatively associated with fasting appetite sensations (except fullness) at the 2nd trimester (p < 0.02, for all). Postprandially, significant associations were observed for incremental areas under the curve from 0 to 30 min between GLP-1 and fullness at the 2nd (p = 0.01) and 3rd trimesters (p = 0.03). No associations between fasting or postprandial GLP-1 and usual energy intake were observed. Overall, GLP-1 and appetite sensation responses significantly differ between trimesters, but few associations were observed between GLP-1, appetite sensations, and usual energy intake.

The effects of sleep disruption on metabolism, hunger, and satiety, and the influence of psychosocial stress and exercise: A narrative review.

Sleep deficiency is a ubiquitous phenomenon among Americans. In fact, in the United States, ∼78% of teens and 35% of adults currently get less sleep than recommended for their age-group, and the quality of sleep appears to be getting worse for many. The consequences of sleep disruption manifest in a myriad of ways, including insulin resistance and disrupted nutrient metabolism, dysregulation of hunger and satiety, and potentially increased body weight and adiposity. Consequently, inadequate sleep is related to an increased risk of various cardiometabolic diseases, including obesity, diabetes, and heart disease. Exercise has the potential to be an effective therapeutic to counteract the deleterious effects of sleep disruption listed above, whereas chronic psychosocial stress may causally promote sleep disruption and cardiometabolic risk. Here, we provide a narrative review of the current evidence on the consequences of short sleep duration and poor sleep quality on substrate metabolism, circulating appetite hormones, hunger and satiety, and weight gain. Secondly, we provide a brief overview of chronic psychosocial stress and its impact on sleep and metabolic health. Finally, we summarise the current evidence regarding the ability of exercise to counteract the adverse metabolic health effects of sleep disruption. Throughout the review, we highlight areas where additional interrogation and future exploration are necessary.

Neurohormonal response patterns to hunger, satiation, and postprandial fullness in normal weight, anorexia nervosa, and obesity.

BACKGROUND: Food intake is regulated by homeostatic and hedonic systems that interact in a complex neuro-hormonal network. Dysregulation in energy intake can lead to obesity (OB) or anorexia nervosa (AN). However, little is known about the neurohormonal response patterns to food intake in normal weight (NW), OB, and AN. MATERIAL & METHODS: During an ad libitum nutrient drink (Ensure®) test (NDT), participants underwent three pseudo-continuous arterial spin labeling (pCASL) MRI scans. The first scan was performed before starting the NDT after a > 12 h overnight fast (Hunger), the second after reaching maximal fullness (Satiation), and the third 30-min after satiation (postprandial fullness). We measured blood levels of ghrelin, cholecystokinin (CCK), glucagon-like peptide (GLP-1), and peptide YY (PYY) with every pCASL-MRI scan. Semiquantitative cerebral blood flow (CBF) maps in mL/100 gr brain/min were calculated and normalized (nCBF) with the CBF in the frontoparietal white matter. The hypothalamus (HT), nucleus accumbens [NAc] and dorsal striatum [DS] were selected as regions of interest (ROIs). RESULTS: A total of 53 participants, 7 with AN, 17 with NW (body-mass index [BMI] 18.5-24.9 kg/m2 ), and 29 with OB (BMI ≥30 kg/m2 ) completed the study. The NW group had a progressive decrease in all five ROIs during the three stages of food intake (hunger, satiation, and post-prandial fullness). In contrast, participants with OB showed a minimal change from hunger to postprandial fullness in all five ROIs. The AN group had a sustained nCBF in the HT and DS, from hunger to satiation, with a subsequent decrease in nCBF from satiation to postprandial fullness. All three groups had similar hormonal response patterns with a decrease in ghrelin, an increase in GLP-1 and PYY, and no change in CCK. CONCLUSION: Conditions of regulated (NW) and dysregulated (OB and AN) energy intake are associated with distinctive neurohormonal activity patterns in response to hunger, satiation, and postprandial fullness.

Pre-prandial plasma liver-expressed antimicrobial peptide 2 (LEAP2) concentration in humans is inversely associated with hunger sensation in a ghrelin independent manner.

PURPOSE: The liver-expressed antimicrobial peptide 2 (LEAP2) is a newly recognized peptide hormone that acts via the growth hormone secretagogue receptor (GHSR) blunting the effects of ghrelin and displaying ghrelin-independent actions. Since the implications of LEAP2 are beginning to be elucidated, we investigated if plasma LEAP2 concentration varies with feeding status or sex and whether it is associated with glucose metabolism and appetite sensations. METHODS: We performed a single test meal study, in which plasma concentrations of LEAP2, ghrelin, insulin and glucose as well as visual analogue scales for hunger, desire to eat, prospective food consumption, fullness were assessed before and 60 min after breakfast in 44 participants (n = 21 females) with normal weight (NW) or overweight/obesity (OW/OB). RESULTS: Pre-prandial plasma LEAP2 concentration was ~ 1.6-fold higher whereas ghrelin was ~ 2.0-fold lower in individuals with OW/OB (p < 0.001) independently of sex. After adjusting for body mass index (BMI) and sex, pre-prandial plasma LEAP2 concentration displayed a direct relationship with BMI (ß: 0.09; 95%CI: 0.05, 0.13; p < 0.001), fat mass (ß: 0.05; 95%CI: 0.01, 0.09; p = 0.010) and glycemia (ß: 0.24; 95%CI: 0.05, 0.43; p = 0.021), whereas plasma ghrelin concentration displayed an inverse relationship with BMI and fat mass but not with glycemia. Postprandial plasma LEAP2 concentration increased ~ 58% in females with OW/OB (p = 0.045) but not in females with NW or in males. Pre-prandial plasma LEAP2 concentration displayed an inverse relationship with hunger score (ß: - 11.16; 95% CI: - 18.52, - 3.79; p = 0.004), in a BMI-, sex- and ghrelin-independent manner. CONCLUSIONS: LEAP2 emerges as a key hormone implicated in the regulation of metabolism and appetite in humans. TRIAL REGISTRATION: The study was retrospectively registered in clinicaltrials.gov (April 2023). CLINICALTRIALS: gov Identifier: NCT05815641.

Anti-inflammatory effects of hunger are transmitted to the periphery via projection-specific AgRP circuits.

Caloric restriction has anti-inflammatory effects. However, the coordinated physiological actions that lead to reduced inflammation in a state of caloric deficit (hunger) are largely unknown. Using a mouse model of injury-induced peripheral inflammation, we find that food deprivation reduces edema, temperature, and cytokine responses that occur after injury. The magnitude of the anti-inflammatory effect that occurs during hunger is more robust than that of non-steroidal anti-inflammatory drugs. The effects of hunger are recapitulated centrally by activity in nutrient-sensing hypothalamic agouti-related protein (AgRP)-expressing neurons. We find that AgRP neurons projecting to the paraventricular nucleus of the hypothalamus rapidly and robustly reduce inflammation and mediate the majority of hunger's anti-inflammatory effects. Intact vagal efferent signaling is required for the anti-inflammatory action of hunger, revealing a brain-to-periphery pathway for this reduction in inflammation. Taken together, these data begin to unravel a potent anti-inflammatory pathway engaged by hypothalamic AgRP neurons to reduce inflammation.

Neural landscape diffusion resolves conflicts between needs across time.

Animals perform flexible goal-directed behaviours to satisfy their basic physiological needs1-12. However, little is known about how unitary behaviours are chosen under conflicting needs. Here we reveal principles by which the brain resolves such conflicts between needs across time. We developed an experimental paradigm in which a hungry and thirsty mouse is given free choices between equidistant food and water. We found that mice collect need-appropriate rewards by structuring their choices into persistent bouts with stochastic transitions. High-density electrophysiological recordings during this behaviour revealed distributed single neuron and neuronal population correlates of a persistent internal goal state guiding future choices of the mouse. We captured these phenomena with a mathematical model describing a global need state that noisily diffuses across a shifting energy landscape. Model simulations successfully predicted behavioural and neural data, including population neural dynamics before choice transitions and in response to optogenetic thirst stimulation. These results provide a general framework for resolving conflicts between needs across time, rooted in the emergent properties of need-dependent state persistence and noise-driven shifts between behavioural goals.

An all 2D bio-inspired gustatory circuit for mimicking physiology and psychology of feeding behavior.

Animal behavior involves complex interactions between physiology and psychology. However, most AI systems neglect psychological factors in decision-making due to a limited understanding of the physiological-psychological connection at the neuronal level. Recent advancements in brain imaging and genetics have uncovered specific neural circuits that regulate behaviors like feeding. By developing neuro-mimetic circuits that incorporate both physiology and psychology, a new emotional-AI paradigm can be established that bridges the gap between humans and machines. This study presents a bio-inspired gustatory circuit that mimics adaptive feeding behavior in humans, considering both physiological states (hunger) and psychological states (appetite). Graphene-based chemitransistors serve as artificial gustatory taste receptors, forming an electronic tongue, while 1L-MoS2 memtransistors construct an electronic-gustatory-cortex comprising a hunger neuron, appetite neuron, and feeding circuit. This work proposes a novel paradigm for emotional neuromorphic systems with broad implications for human health. The concept of gustatory emotional intelligence can extend to other sensory systems, benefiting future humanoid AI.

Toggling between food-seeking and self-preservation behaviors via hypothalamic response networks.

Motivated behaviors are often studied in isolation to assess labeled lines of neural connections underlying innate actions. However, in nature, multiple systems compete for expression of goal-directed behaviors via complex neural networks. Here, we examined flexible survival decisions in animals tasked with food seeking under predation threat. We found that predator exposure rapidly induced physiological, neuronal, and behavioral adaptations in mice highlighted by reduced food seeking and consumption contingent on current threat level. Diminishing conflict via internal state or external environment perturbations shifted feeding strategies. Predator introduction and/or selective manipulation of danger-responsive cholecystokinin (Cck) cells of the dorsal premammilary nucleus (PMd) suppressed hunger-sensitive Agouti-related peptide (AgRP) neurons, providing a mechanism for threat-evoked hypophagia. Increased caloric need enhanced food seeking under duress through AgRP pathways to the bed nucleus of the stria terminalis (BNST) and/or lateral hypothalamus (LH). Our results suggest oscillating interactions between systems underlying self-preservation and food seeking to promote optimal behavior.

Daily ovarian hormone exposure and loss of control eating in adolescent girls: A registered report.

OBJECTIVE: The daily biobehavioral factors that precipitate loss of control eating (LOCE) in adolescent girls are not well known. Ovarian hormone levels are key biological factors associated with the etiology of eating disorders in adolescent girls. Yet, models on how daily ovarian hormone exposure predicts LOCE in adolescent girls are underdeveloped. The goal of this study is to examine the daily patterns and mechanisms of ovarian hormone levels on LOCE across the menstrual cycle in adolescent girls and the mediating roles of food-related reward anticipation and response inhibition. Ecological momentary assessment (EMA) paired with daily hormonal sampling will be used to examine (1) daily associations between within-person hormones and LOCE, and (2) the mediating role of within-person food-related reward anticipation and response inhibition. METHODS: Normally cycling adolescent girls who have reached menarche will provide daily saliva samples for hormone analysis and complete EMA for 35 days. During EMA, girls will report LOCE and will complete task-based and self-report measures of food-related response inhibition and reward anticipation. DISCUSSION: This work has implications for the development of new real-world biobehavioral models of LOCE in adolescent girls, which will guide theory improvements and treatment for LOCE. Results will provide preliminary evidence for treatment targets for novel interventions for adolescent girls-for example, a response inhibition intervention. PUBLIC SIGNIFICANCE: Adolescent eating disorders are severe mental health conditions, often marked by loss of control eating. Estrogen and progesterone play a role in the development and persistence of loss of control eating. The current study will examine how daily exposure to estrogen and progesterone predicts loss of control eating in adolescent girls and identify possible daily mechanisms linking estrogen and progesterone exposure and loss of control eating.

Behavioral dissection of hunger states in Drosophila.

Hunger is a motivational drive that promotes feeding, and it can be generated by the physiological need to consume nutrients as well as the hedonic properties of food. Brain circuits and mechanisms that regulate feeding have been described, but which of these contribute to the generation of motive forces that drive feeding is unclear. Here, we describe our first efforts at behaviorally and neuronally distinguishing hedonic from homeostatic hunger states in Drosophila melanogaster and propose that this system can be used as a model to dissect the molecular mechanisms that underlie feeding motivation. We visually identify and quantify behaviors exhibited by hungry flies and find that increased feeding duration is a behavioral signature of hedonic feeding motivation. Using a genetically encoded marker of neuronal activity, we find that the mushroom body (MB) lobes are activated by hedonic food environments, and we use optogenetic inhibition to implicate a dopaminergic neuron cluster (protocerebral anterior medial [PAM]) to α'/ß' MB circuit in hedonic feeding motivation. The identification of discrete hunger states in flies and the development of behavioral assays to measure them offers a framework to begin dissecting the molecular and circuit mechanisms that generate motivational states in the brain.

Food approach dynamics in daily life: Speed and force of food approach movements fluctuate with hunger, but less so for people with high BMI.

Researchers have suggested that the overconsumption of food, alcohol, and drugs could be explained by chronically elevated approach tendencies to rewarding but unhealthy stimuli. Here, we use the example of food to show that dysregulated rather than chronically elevated approach tendencies are associated with adverse health outcomes. To this end, we developed a new smartphone-based paradigm to measure dynamic changes in food approach tendencies outside the laboratory (piloted with n = 48). We demonstrated in three preregistered experiments (total N = 367) that food approach tendencies decrease from before to after people have eaten. We further show that in overweight and obese participants, these dynamics are disrupted as their food approach tendencies increase rather than decrease after meals. In addition to showing these effects based on traditional reaction time-based food approach tendencies, we also demonstrate these patterns in a novel measure of response force-a measure that has long been used to study motivation in animals but has received little attention in humans. Together, our findings suggest that both reaction time-based and force-based approach tendencies change dynamically in accordance with people's need states and that disruptions in these dynamics are associated with adverse health outcomes, such as overweight and obesity. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

A qualitative exploration of perceived barriers and facilitators to following an intuitive eating style.

BACKGROUND: Intuitive eating involves following internal cues of hunger and satiety to guide eating choices as opposed to responding to external signals, strong emotions, or dietary rules. This style of eating has consistently been shown to be related to better physical and psychological health indicators, and more interventions are being designed and studied to promote this eating style. The current study aimed to identify anticipated facilitators and barriers to following this style of eating among a group of college students enrolled in a larger study of intuitive eating. METHOD: Following a week of tracking their current eating as part of a larger study, college students read a description of intuitive eating. They then answered three open-ended questions about following intuitive eating including facilitators, barriers, and perceived ability to follow long term. Responses were coded using thematic analysis to identify themes across responses. RESULTS: Among 100 participants, 86 % were female, 46 % were Hispanic (41 % non-Hispanic White, 13 % other race/ethnicity), mean age was 24.3 years, and mean body mass index was 26.2. The most commonly anticipated participant-reported facilitators of intuitive eating were being in touch with the body's needs and hunger cues, positive perceptions of intuitive eating, and health considerations. The most commonly anticipated barriers were logistical constraints (e.g., busyness and mealtimes), difficulty with hunger cues and reactions to food, and negative perceptions of intuitive eating. The majority of participants (64 %) would consider following this style of eating long term. DISCUSSION: This study provides information that can be used to improve efforts aimed at promoting intuitive eating to college students, including marketing intuitive eating interventions, and clarifying misunderstandings of its key tenets that might serve as barriers.

Effects of hunger on neuronal histone modifications slow aging in Drosophila.

Hunger is an ancient drive, yet the molecular nature of pressures of this sort and how they modulate physiology are unknown. We find that hunger modulates aging in Drosophila. Limitation of branched-chain amino acids (BCAAs) or activation of hunger-promoting neurons induced a hunger state that extended life span despite increased feeding. Alteration of the neuronal histone acetylome was associated with BCAA limitation, and preventing these alterations abrogated the effect of BCAA limitation to increase feeding and extend life span. Hunger acutely increased feeding through usage of the histone variant H3.3, whereas prolonged hunger seemed to decrease a hunger set point, resulting in beneficial consequences for aging. Demonstration of the sufficiency of hunger to extend life span reveals that motivational states alone can be deterministic drivers of aging.