Genetic Identification of Vagal Sensory Neurons That Control Feeding.

Energy homeostasis requires precise measurement of the quantity and quality of ingested food. The vagus nerve innervates the gut and can detect diverse interoceptive cues, but the identity of the key sensory neurons and corresponding signals that regulate food intake remains unknown. Here, we use an approach for target-specific, single-cell RNA sequencing to generate a map of the vagal cell types that innervate the gastrointestinal tract. We show that unique molecular markers identify vagal neurons with distinct innervation patterns, sensory endings, and function. Surprisingly, we find that food intake is most sensitive to stimulation of mechanoreceptors in the intestine, whereas nutrient-activated mucosal afferents have no effect. Peripheral manipulations combined with central recordings reveal that intestinal mechanoreceptors, but not other cell types, potently and durably inhibit hunger-promoting AgRP neurons in the hypothalamus. These findings identify a key role for intestinal mechanoreceptors in the regulation of feeding.

Secretin-Activated Brown Fat Mediates Prandial Thermogenesis to Induce Satiation.

The molecular mediator and functional significance of meal-associated brown fat (BAT) thermogenesis remains elusive. Here, we identified the gut hormone secretin as a non-sympathetic BAT activator mediating prandial thermogenesis, which consequentially induces satiation, thereby establishing a gut-secretin-BAT-brain axis in mammals with a physiological role of prandial thermogenesis in the control of satiation. Mechanistically, meal-associated rise in circulating secretin activates BAT thermogenesis by stimulating lipolysis upon binding to secretin receptors in brown adipocytes, which is sensed in the brain and promotes satiation. Chronic infusion of a modified human secretin transiently elevates energy expenditure in diet-induced obese mice. Clinical trials with human subjects showed that thermogenesis after a single-meal ingestion correlated with postprandial secretin levels and that secretin infusions increased glucose uptake in BAT. Collectively, our findings highlight the largely unappreciated function of BAT in the control of satiation and qualify BAT as an even more attractive target for treating obesity.

Income and emotional well-being: A conflict resolved.

Do larger incomes make people happier? Two authors of the present paper have published contradictory answers. Using dichotomous questions about the preceding day, [Kahneman and Deaton, Proc. Natl. Acad. Sci. U.S.A. 107, 16489-16493 (2010)] reported a flattening pattern: happiness increased steadily with log(income) up to a threshold and then plateaued. Using experience sampling with a continuous scale, [Killingsworth, Proc. Natl. Acad. Sci. U.S.A. 118, e2016976118 (2021)] reported a linear-log pattern in which average happiness rose consistently with log(income). We engaged in an adversarial collaboration to search for a coherent interpretation of both studies. A reanalysis of Killingsworth's experienced sampling data confirmed the flattening pattern only for the least happy people. Happiness increases steadily with log(income) among happier people, and even accelerates in the happiest group. Complementary nonlinearities contribute to the overall linear-log relationship. We then explain why Kahneman and Deaton overstated the flattening pattern and why Killingsworth failed to find it. We suggest that Kahneman and Deaton might have reached the correct conclusion if they had described their results in terms of unhappiness rather than happiness; their measures could not discriminate among degrees of happiness because of a ceiling effect. The authors of both studies failed to anticipate that increased income is associated with systematic changes in the shape of the happiness distribution. The mislabeling of the dependent variable and the incorrect assumption of homogeneity were consequences of practices that are standard in social science but should be questioned more often. We flag the benefits of adversarial collaboration.

Maternal depressive symptom trajectories and associations with child feeding.

BACKGROUND: Responsive feeding, when caregivers attend to children's signals of hunger and satiation and respond in an emotionally supportive and developmentally appropriate way, is associated with the development of healthy eating behaviors, improved diet quality, and healthy weight status for children. However, gaps in the literature remain on how factors, such as maternal depressive symptoms and child temperament, influence feeding interactions. METHODS: This longitudinal secondary data analysis explored the association between maternal depressive symptom trajectory and child temperament with maternal feeding practices in women with obesity who participated in a prenatal lifestyle intervention trial. Mothers self-reported depressive symptoms at baseline, 35 weeks gestation, and 6, 12, and 18 months postpartum. At 18- and 24-months postpartum, mothers completed self-reported assessments of feeding practices and child temperament and completed in-home video-recorded meals with their child, coded using the Responsiveness to Child Feeding Cues Scale. We used group-based trajectory modeling to identify distinct trajectories of depressive symptoms and generalized regressions to assess the association between symptom trajectory group and feeding. We also explored interactions between depressive symptoms and child temperament. RESULTS: Three distinct trajectories of depressive symptoms were identified: No-Minimal and Decreasing, Mild-Moderate and Stable, and Moderate-Severe and Stable. At 18-months, when compared to the No-Minimal and Decreasing group, membership in the Moderate-Severe and Stable group was associated with higher observed responsiveness to child satiation cues ([Formula: see text] =2.3, 95%CI = 0.2, 4.4) and lower self-reported pressure to eat ([Formula: see text]=-0.4, 95%CI= -0.7, 0.0). When compared to the No-Minimal and Decreasing group, membership in the Mild-Moderate and Stable group was associated with higher self-reported restriction ([Formula: see text] =0.4, 95%CI = 0.0,0.7). The associations between trajectory group membership and feeding practices did not reach statistical significance at 24 months. Associations between depressive symptoms and restriction were moderated by child effortful control at 18 months [Formula: see text]) and surgency at 24 months [Formula: see text]). CONCLUSION: A Moderate-Severe and Stable depressive symptom trajectory was associated with more responsive feeding practices and a Mild-Moderate and Stable trajectory was associated with higher restrictive feeding. Preliminary evidence suggests that depressive symptoms impact mothers' ability to match their use of restriction to the temperamental needs of their child.

Not feeling the heat? Effects of dietary protein on satiation and satiety in mice are not due to its impact on body temperature.

Dietary protein modulates food intake (FI) via unclear mechanism(s). One possibility is that higher protein leads to greater post-ingestive heat production (Specific dynamic action: SDA) leading to earlier meal termination (increased satiation), and inhibition of further intake (increased satiety). The influence of dietary protein on feeding behaviour in C57BL/6J mice was tested using an automated FI monitoring system (BioDAQ), simultaneous to body temperature (Tb). Total FI, inter meal intervals (IMI, satiety) and meal size (MS, satiation) were related to changes in Tb after consuming low (5%, LP), moderate (15%, MP) and high (30%, HP) protein diets. Diets were tested over three conditions: 1) room temperature (RT, 21 ± 1 °C), 2) room temperature and running wheels (RTRW) and 3) low temperature (10 °C) and running wheels (LTRW). The differences between diets and conditions were also compared using mixed models. Mice housed at RT fed HP diet, reduced total FI compared with LP and MP due to earlier meal termination (satiation effect). FI was lowered in RTRW conditions with no differences between diets. FI significantly increased under LTRW conditions for all diets, with protein content leading to earlier meal termination (satiation) but not the intervals between feeding bouts (satiety). Tb fell immediately after feeding in all conditions. Despite a reduction in total FI in mice fed HP, mediated via increased satiation, this effect was not linked to increased Tb during meals. We conclude effects of dietary protein on intake are not mediated via SDA and Tb.

Reasons for meal termination, eating frequency, and typical meal context differ between persons with and without a spinal cord injury.

Overeating associated with neurogenic obesity after spinal cord injury (SCI) may be related to how persons with SCI experience satiation (processes leading to meal termination), their eating frequency, and the context in which they eat their meals. In an online, cross-sectional study, adults with (n = 688) and without (Controls; n = 420) SCI completed the Reasons Individuals Stop Eating Questionnaire-15 (RISE-Q-15), which measures individual differences in the experience of factors contributing to meal termination on five scales: Physical Satisfaction, Planned Amount, Decreased Food Appeal, Self-Consciousness, and Decreased Priority of Eating. Participants also reported weekly meal and snack frequency and who prepares, serves, and eats dinner with them at a typical dinner meal. Analysis revealed that while Physical Satisfaction, Planned Amount, and Decreased Food Appeal were reported as the most frequent drivers of meal termination in both groups, scores for the RISE-Q-15 scales differed across the groups. Compared to Controls, persons with SCI reported Physical Satisfaction and Planned Amount as drivers of meal termination less frequently, and Decreased Food Appeal and Decreased Priority of Eating more frequently (all p < 0.001). This suggests that persons with SCI rely less on physiological satiation cues for meal termination than Controls and instead rely more on hedonic cues. Compared to Controls, persons with SCI less frequently reported preparing and serving dinner meals and less frequently reported eating alone (all p < 0.001), indicating differences in meal contexts between groups. Individuals with SCI reported consuming fewer meals than Controls but reported a higher overall eating frequency due to increased snacking (p ≤ 0.015). A decrease in the experience of physical fullness, along with a dependence on a communal meal context and frequent snacking, likely contribute to overeating associated with neurogenic obesity after SCI.

Meat- and plant-based products induced similar satiation which was not affected by multimodal augmentation.

Little is known about how plant-based products influence satiation compared to corresponding meat-based products. As augmented reality (AR) intensifies sensory experiences, it was hypothesized to improve satiation. This study compared satiation between intake of meatballs and plant-based balls and plant-based balls intensified with AR for visual, olfactory, and haptic sensory properties. Intake order of the meatballs, plant-based balls, and augmented plant-based balls, eaten on separate days, was randomized. Satiation was measured from twenty-eight non-obese adults as ad libitum intake of the balls and extra snacks, and as subjective appetite sensations. Liking and wanting to eat the products were also investigated. There were no differences between the products in satiation. Before tasting the augmented plant-based balls were less liked than the meatballs (p = 0.002) or plant-based balls (p = 0.046), but after eating the first ball or eating the ad libitum number of balls the differences in liking disappeared. Wanting evaluations were similar for each product and decreased during eating (p < 0.001). A group of participants susceptible to AR was found (n = 11), described by decreased intake when augmentation was applied. Among the sub-group, wanting to eat the augmented balls was lower before tasting (p = 0.019) and after eating the first ball (p = 0.002) and appetite was less suppressed after eating the balls ad libitum (p = 0.01), when compared to non-susceptible participants. We conclude that meatballs and plant-based balls were equal in inducing satiation, and multisensory augmentation did not influence satiation. However, the augmentation decreased liking evaluations before tasting. Further studies are needed to explore differences between consumer groups in susceptibility to augmentation.

Experienced well-being rises with income, even above $75,000 per year.

What is the relationship between money and well-being? Research distinguishes between two forms of well-being: people's feelings during the moments of life (experienced well-being) and people's evaluation of their lives when they pause and reflect (evaluative well-being). Drawing on 1,725,994 experience-sampling reports from 33,391 employed US adults, the present results show that both experienced and evaluative well-being increased linearly with log(income), with an equally steep slope for higher earners as for lower earners. There was no evidence for an experienced well-being plateau above $75,000/y, contrary to some influential past research. There was also no evidence of an income threshold at which experienced and evaluative well-being diverged, suggesting that higher incomes are associated with both feeling better day-to-day and being more satisfied with life overall.

Slc12a2 loss in insulin-secreting ß-cells links development of overweight and metabolic dysregulation to impaired satiation control of feeding.

Male mice lacking the Na+-K+-2Cl- cotransporter Slc12a2 (Nkcc1) specifically in insulin-secreting ß-cells (Slc12a2ßKO) have reduced ß-cell mass and mild ß-cell secretory dysfunction associated with overweight, glucose intolerance, insulin resistance, and metabolic abnormalities. Here, we confirmed and extended previous results to female Slc12a2ßKO mice, which developed a similar metabolic syndrome-like phenotype as males, albeit milder. Notably, male and female Slc12a2ßKO mice developed overweight without consuming excess calories. Analysis of the feeding microstructure revealed that young lean Slc12a2ßKO male mice ate meals of higher caloric content and at a relatively lower frequency than normal mice, particularly during the night. In addition, overweight Slc12a2ßKO mice consumed significantly larger meals than lean mice. Therefore, the reduced satiation control of feeding precedes the onset of overweight and is worsened in older Slc12a2ßKO mice. However, the time spent between meals remained intact in lean and overweight Slc12a2ßKO mice, indicating conserved satiety responses to ad libitum feeding. Nevertheless, satiety was intensified during and after refeeding only in overweight males. In lean females, satiety responses to refeeding were delayed relative to age- and body weight-matched control mice but normalized in overweight mice. Since meal size did not change during refeeding, these data suggested that the satiety control of eating after fasting is impaired in lean Slc12a2ßKO mice before the onset of overweight and independently of their reduced satiation responses. Therefore, our results support the novel hypothesis that reduced satiation precedes the onset of overweight and the development of metabolic dysregulation.NEW & NOTEWORTHY Obesity, defined as excess fat accumulation, increases the absolute risk for metabolic diseases. Although obesity is usually attributed to increased food intake, we demonstrate that body weight gain can be hastened without consuming excess calories. In fact, impaired meal termination control, i.e., satiation, is detectable before the development of overweight in an animal model that develops a metabolic syndrome-like phenotype.

Feeding signals inhibit fluid-satiation signals in the mouse lateral parabrachial nucleus to increase intake of highly palatable, caloric solutions.

Chemogenetic activation of oxytocin receptor-expressing neurons in the parabrachial nucleus (OxtrPBN neurons) acts as a satiation signal for water. In this research, we investigated the effect of activating OxtrPBN neurons on satiation for different types of fluids. Chemogenetic activation of OxtrPBN neurons in male and female transgenic OxtrCre mice robustly suppressed the rapid, initial (15-min) intake of several solutions after dehydration: water, sucrose, ethanol and saccharin, but only slightly decreased intake of Ensure®, a highly caloric solution (1 kcal/mL; containing 3.72 g protein, 3.27 g fat, 13.42 g carbohydrates, and 1.01 g dietary fibre per 100 mL). OxtrPBN neuron activation also suppressed cumulative, longer-term (2-h) intake of lower caloric, less palatable solutions, but not highly caloric, palatable solutions. These results suggest that OxtrPBN neurons predominantly control initial fluid-satiation responses after rehydration, but not longer-term intake of highly caloric, palatable solutions. The suppression of fluid intake was not because of anxiogenesis, but because OxtrPBN neuron activation decreased anxiety-like behaviour. To investigate the role of different PBN subdivisions on the intake of different solutions, we examined FOS as a proxy marker of PBN neuron activation. Different PBN subdivisions were activated by different solutions: the dorsolateral PBN similarly by all fluids; the external lateral PBN by caloric but not non-caloric solutions; and the central lateral PBN primarily by highly palatable solutions, suggesting PBN subdivisions regulate different aspects of fluid intake. To explore the possible mechanisms underlying the minimal suppression of Ensure® after OxtrPBN neuron activation, we demonstrated in in vitro slice recordings that the feeding-associated agouti-related peptide (AgRP) inhibited OxtrPBN neuron firing in a concentration-related manner, suggesting possible inhibition by feeding-related neurocircuitry of fluid satiation neurocircuitry. Overall, this research suggests that although palatable beverages like sucrose- and ethanol-containing beverages activate fluid satiation signals encoded by OxtrPBN neurons, these neurons can be inhibited by hunger-related signals (agouti-related peptide, AgRP), which may explain why these fluids are often consumed in excess of what is required for fluid satiation.

A Randomized, Controlled Trial of Efficacy and Safety of Cannabidiol in Idiopathic and Diabetic Gastroparesis.

BACKGROUND & AIMS: Cannabis (delta-9-tetrahydrocannabinol), a nonselective cannabinoid-receptor agonist, relieves nausea and pain. Cannabidiol (CBD), a cannabinoid receptor 2 inverse agonist with central effects, also reduces gut sensation and inflammation. We compared the effects of 4 weeks of treatment with pharmaceutical CBD vs placebo in patients with idiopathic or diabetic (diabetes mellitus) gastroparesis. METHODS: We performed a randomized, double-blinded, placebo-controlled study of CBD twice daily (Epidiolex escalated to 20 mg/kg/d; Jazz Pharmaceuticals, Dublin, Ireland) in patients with nonsurgical gastroparesis with delayed gastric emptying of solids (GES). Symptoms were assessed by the Gastroparesis Cardinal Symptom Index Daily Diary. After 4 weeks of treatment, we measured GES, gastric volumes, and Ensure (Abbott Laboratories, Abbott Park, IL) satiation test (1 kcal/mL, 30 mL/min) to assess volume to comfortable fullness and maximum tolerance. Patients underwent specific FAAH and CNR1 genotyping. Statistical analysis compared 2 treatments using analysis of variance including baseline measurements and body mass index as covariates. RESULTS: Among 44 patients (32 idiopathic, 6 diabetes mellitus type 1, and 6 diabetes mellitus type 2), 5 patients did not tolerate full-dose escalation; 3 withdrew before completing 4 weeks of treatment (2 placebo, 1 CBD); 95% completed 4 weeks of treatment and diaries. Compared with placebo, CBD reduced the total Gastroparesis Cardinal Symptom Index score (P = .008), inability to finish a normal-sized meal (P = .029), number of vomiting episodes/24 hours (P = .006), and overall symptom severity (P = .034). Patients treated with CBD had a higher volume to comfortable fullness and maximum tolerance and slower GES. FAAH rs34420 genotype significantly impacted nutrient drink ingestion. The most common adverse events reported were diarrhea (14 patients), fatigue (8 patients), headache (8 patients), and nausea (7 patients). CONCLUSIONS: CBD provides symptom relief in patients with gastroparesis and improves the tolerance of liquid nutrient intake, despite slowing of GES. CLINICALTRIALS: gov NCT #03941288.

Hindbrain ghrelin and liver-expressed antimicrobial peptide 2, ligands for growth hormone secretagogue receptor, bidirectionally control food intake.

Hindbrain growth hormone secretagogue receptor (GHSR) agonism increases food intake, yet the underlying neural mechanisms remain unclear. The functional effects of hindbrain GHSR antagonism by its endogenous antagonist liver-expressed antimicrobial peptide 2 (LEAP2) are also yet unexplored. To test the hypothesis that hindbrain GHSR agonism attenuates the food intake inhibitory effect of gastrointestinal (GI) satiation signals, ghrelin (at a feeding subthreshold dose) was administered to the fourth ventricle (4V) or directly to the nucleus tractus solitarius (NTS) before systemic delivery of the GI satiation signal cholecystokinin (CCK). Also examined, was whether hindbrain GHSR agonism attenuated CCK-induced NTS neural activation (c-Fos immunofluorescence). To investigate an alternate hypothesis that hindbrain GHSR agonism enhances feeding motivation and food seeking, intake stimulatory ghrelin doses were administered to the 4V and fixed ratio 5 (FR-5), progressive ratio (PR), and operant reinstatement paradigms for palatable food responding were evaluated. Also assessed were 4V LEAP2 delivery on food intake and body weight (BW) and on ghrelin-stimulated feeding. Both 4V and NTS ghrelin blocked the intake inhibitory effect of CCK and 4V ghrelin blocked CCK-induced NTS neural activation. Although 4V ghrelin increased low-demand FR-5 responding, it did not increase high-demand PR or reinstatement of operant responding. Fourth ventricle LEAP2 reduced chow intake and BW and blocked hindbrain ghrelin-stimulated feeding. Data support a role for hindbrain GHSR in bidirectional control of food intake through mechanisms that include interacting with the NTS neural processing of GI satiation signals but not food motivation and food seeking.

Secretin modulates appetite via brown adipose tissue-brain axis.

PURPOSE: Secretin activates brown adipose tissue (BAT) and induces satiation in both mice and humans. However, the exact brain mechanism of this satiety inducing, secretin-mediated gut-BAT-brain axis is largely unknown. METHODS AND RESULTS: In this placebo-controlled, single-blinded neuroimaging study, firstly using [18F]-fluorodeoxyglucose (FDG) PET measures (n = 15), we established that secretin modulated brain glucose consumption through the BAT-brain axis. Predominantly, we found that BAT and caudate glucose uptake levels were negatively correlated (r = -0.54, p = 0.037) during secretin but not placebo condition. Then, using functional magnetic resonance imaging (fMRI; n = 14), we found that secretin improved inhibitory control and downregulated the brain response to appetizing food images. Finally, in a PET-fMRI fusion analysis (n = 10), we disclosed the patterned correspondence between caudate glucose uptake and neuroactivity to reward and inhibition, showing that the secretin-induced neurometabolic coupling patterns promoted satiation. CONCLUSION: These findings suggest that secretin may modulate the BAT-brain metabolic crosstalk and subsequently the neurometabolic coupling to induce satiation. The study advances our understanding of the secretin signaling in motivated eating behavior and highlights the potential role of secretin in treating eating disorders and obesity. TRIAL REGISTRATION: EudraCT no. 2016-002373-35, registered 2 June 2016; Clinical Trials no. NCT03290846, registered 25 September 2017.

Protein Source Influences Acute Appetite and Satiety but Not Subsequent Food Intake in Healthy Adults.

BACKGROUND: Although current recommendations encourage plant-based dietary patterns, data is limited as to whether the equivalent substitution of animal-based protein-rich foods with plant-based versions impacts ingestive behavior. OBJECTIVES: To compare higher-protein preloads, varying in protein source, on appetite, satiety, and subsequent energy intake. METHODS: Thirty-two adults (age: 25 ± 1 y; body mass index (BMI) measured in kg/m2: 24.2 ± 0.5 kg/m2) randomly consumed 250 kcal, protein-preload beverages (24 g protein), varying in protein source [whey, soy, and pea protein isolates (WHEY, SOY, and PEA) or micellar casein (CAS)] each morning for 3 acclimation days/preload. On day 4, participants completed a 4-h clinical testing day in which the respective preload was consumed, followed by blood sampling and questionnaires every 30 min for appetite and satiety. In addition, an ad libitum lunch was provided 4-h postpreload. On day 5, participants consumed the respective preload at home, followed by an ad libitum breakfast 30 min afterward. For normally-distributed data, repeated-measures analysis of variance (ANOVA) or Friedman nonparametric test were utilized to compare the main effects of protein source on study outcomes. Post hoc pairwise comparisons using least-significant differences (LSD) were then performed. RESULTS: CAS (-3330 ± 690 mm∗240 min) and PEA (-2840 ± 930mm∗240 min) reduced 4-h appetite compared with SOY (-1440 ± 936 mm∗240 min; both, P < 0.05). WHEY was not different (-2290 ± 930 mm∗240 min). CAS (3520 ± 84 pg/mL∗240 min) and PEA (3860 ± 864 pg/mL∗240 min) increased 4-h peptide YY concentrations compared with SOY (2200 ± 869 pg/mL∗240 min; both, P < 0.05). WHEY was not different (3870 ± 932 pg/mL∗240 min). No differences in ad libitum energy intake were observed. CONCLUSIONS: CAS and PEA, but not WHEY, elicited greater acute changes in appetite and satiety compared with SOY in healthy adults, supporting that not all protein sources are equivalent. This trial is registered at clinicaltrials.gov (NCT03154606).

Cerebellar Prediction and Feeding Behaviour.

Given the importance of the cerebellum in controlling movements, it might be expected that its main role in eating would be the control of motor elements such as chewing and swallowing. Whilst such functions are clearly important, there is more to eating than these actions, and more to the cerebellum than motor control. This review will present evidence that the cerebellum contributes to homeostatic, motor, rewarding and affective aspects of food consumption.Prediction and feedback underlie many elements of eating, as food consumption is influenced by expectation. For example, circadian clocks cause hunger in anticipation of a meal, and food consumption causes feedback signals which induce satiety. Similarly, the sight and smell of food generate an expectation of what that food will taste like, and its actual taste will generate an internal reward value which will be compared to that expectation. Cerebellar learning is widely thought to involve feed-forward predictions to compare expected outcomes to sensory feedback. We therefore propose that the overarching role of the cerebellum in eating is to respond to prediction errors arising across the homeostatic, motor, cognitive, and affective domains.

Influence of eating with distractors on caloric intake of children and adolescents: a systematic review and meta-analysis of interventional controlled studies.

Eating habits developed during childhood can be perpetuated along life and contribute to the emergence of disorders. We aimed to investigate the influence of distractors during experimental meals on the energy intake of children and adolescents. We followed the PRISMA guidelines and the study was registered in PROSPERO (CRD42021259946). The PICOS strategy consisted of children and adolescents (P), exposed to distractors during meals (I), compared with no distraction (C) and the outcome was energy intake (Kcal) (O) evaluated in crossover and parallel randomized clinical trials (RCTs) (S). Searches were conducted in PubMed, Scopus, Web of Science, Cochrane, Proquest, Embase, and LILACs databases. We employed RoB 2 tool and NutriGrade. Databases searches returned 9,576 references. Thirteen articles were selected (five crossover and eight parallel RCTs). Volunteers aged 3 to 17 years-old. All studies evaluated TV as distractor. Most studies presented high/moderate risk of bias. Meta-analysis of parallel RCT indicated no significant difference in energy intake while eating with TV (MD = 0.05; 95% CI -0.13 - 0.23, P = 0.57), with moderate certainty level. In conclusion, under laboratory conditions, eating with distractors seems to barely alter energy intake for children and adolescents.Supplemental data for this article is available online at https://doi.org/10.1080/10408398.2022.2055525 .

Preliminary data that psychological treatment and baseline anxiety are associated with a decrease in postprandial fullness and early satiation for individuals with bulimia nervosa and related other specified feeding or eating disorder.

OBJECTIVE: Gastrointestinal symptoms, particularly postprandial fullness, are frequently reported in eating disorders. Limited data exist evaluating how these symptoms change in response to outpatient psychological treatment. The current study sought to describe the course of postprandial fullness and early satiation across psychological treatment for adults with bulimia nervosa and related other specified feeding or eating disorders and to test if anxiety moderates treatment response. METHODS: Secondary data analysis was conducted on questionnaire data provided by 30 individuals (80% white, M(SD)age = 31.43(13.44) years; 90% female) throughout treatment and six-month follow-up in a pilot trial comparing mindfulness and acceptance-based treatment with cognitive-behavioral therapy for bulimia nervosa. Participants completed items from the Rome IV Diagnostic Questionnaire for Adult Functional Gastrointestinal Disorders and the State Trait Anxiety Inventory. RESULTS: Postprandial fullness and early satiation both significantly decreased over time (ds = 1.23-1.54; p's < .001). Baseline trait anxiety moderated this outcome, such that greater decreases were observed for those with higher baseline anxiety (p = .02). DISCUSSION: Results extend prior work in inpatient samples by providing preliminary data that postprandial fullness and early satiation decrease with outpatient psychological treatment for bulimia nervosa. Baseline anxiety moderated this effect for postprandial fullness. Future work should replicate findings in a larger sample and test anxiety as a mechanism underlying postprandial fullness in eating disorders. PUBLIC SIGNIFICANCE: The current study found that common gastrointestinal symptoms (postprandial fullness and early satiation) decrease over the course of outpatient psychotherapy for adults with full and subthreshold bulimia nervosa. Postprandial fullness decreased more across time for those high in anxiety.

Longitudinal patterns of breastfeeding and its association with adiposity and subjective indicators of satiety/appetite in the first 2 years of life.

Evidence about the association between breastfeeding and its duration with growth, appetite and satiety indicators, and adiposity in low and middle-income countries facing nutritional transition is scarce. The aim of this study was to evaluate the association between longitudinal patterns of breastfeeding (exclusive [EBF] and continued [CBF]) with adiposity and growth, and the mediating role of appetite and satiety indicators in these associations in Mexican children during the first 2 years of life. Information from 378 mother-child pairs from the MAS-Lactancia birth cohort was analysed. Information was collected at birth and at months 1, 3, 6, 9, 12, 18 and 24 of life. Duration of EBF and CBF was computed. Linear mixed models were used to assess the association of EBF and CBF with growth and adiposity. Path analysis was used for mediation analysis. Compared with the reference group (EBF duration <1 month), males with >3 to ≤6 months of EBF had less abdominal circumference (ß = -0.66, p = 0.05), Z-score weight-for-length (ß = -0.17, p = 0.19) and length-for-age (ß = -0.49, p < 0.01). Participants without CBF beyond 6 months had higher BMI Z-score (ß = 0.19, p < 0.01), abdominal circumference (ß = 0.62, p < 0.01) and skinfold sum (ß = 0.80, p = 0.09), and o difference in length-for-age. For EBF, mediation was confirmed for satiety responsiveness on the association with BMI Z-Score, for food fussiness for the association with abdominal circumference and length-for-age Z-score, and enjoyment of food on the association with length-for-age Z-score. For CBF, mediation was confirmed for food fussiness in the association with length-for-age. This study suggests that a longer exposure to EBF and CBF is associated with lower adiposity in children under 2 years of age, and that this association could be partially mediated by appetite and satiety indicators.

The Role of D-allulose and Erythritol on the Activity of the Gut Sweet Taste Receptor and Gastrointestinal Satiation Hormone Release in Humans: A Randomized, Controlled Trial.

BACKGROUND: Glucose induces the release of gastrointestinal (GI) satiation hormones, such as glucagon-like peptide 1 (GLP-1) and peptide tyrosine tyrosine (PYY), in part via the activation of the gut sweet taste receptor (T1R2/T1R3). OBJECTIVES: The primary objective was to investigate the importance of T1R2/T1R3 for the release of cholecystokinin (CCK), GLP-1, and PYY in response to D-allulose and erythritol by assessing the effect of the T1R2/T1R3 antagonist lactisole on these responses and as secondary objectives to study the effect of the T1R2/T1R3 blockade on gastric emptying, appetite-related sensations, and GI symptoms. METHODS: In this randomized, controlled, double-blind, crossover study, 18 participants (5 men) with a mean ± SD BMI (in kg/m2) of 21.9 ± 1.7 and aged 24 ± 4 y received an intragastric administration of 25 g D-allulose, 50 g erythritol, or tap water, with or without 450 parts per million (ppm) lactisole, respectively, in 6 different sessions. 13C-sodium acetate was added to all solutions to determine gastric emptying. At fixed time intervals, blood and breath samples were collected, and appetite-related sensations and GI symptoms were assessed. Data were analyzed with linear mixed-model analysis. RESULTS: D-allulose and erythritol induced a significant release of CCK, GLP-1, and PYY compared with tap water (all PHolm < 0.0001, dz >1). Lactisole did not affect the D-allulose- and erythritol-induced release of CCK, GLP-1, and PYY (all PHolm > 0.1). Erythritol significantly delayed gastric emptying, increased fullness, and decreased prospective food consumption compared with tap water (PHolm = 0.0002, dz = -1.05; PHolm = 0.0190, dz = 0.69; and PHolm = 0.0442, dz = -0.62, respectively). CONCLUSIONS: D-allulose and erythritol stimulate the secretion of GI satiation hormones in humans. Lactisole had no effect on CCK, GLP-1, and PYY release, indicating that D-allulose- and erythritol-induced GI satiation hormone release is not mediated via T1R2/T1R3 in the gut.

The selective advantage of mast flowering in Veratrum album subsp. oxysepalum: Implications of the predator satiation hypothesis.

PREMISE: Synchronous, highly variable flower or seed production among years within a population (i.e., masting) has been reported in numerous perennial plants. Although masting provides ecological advantages such as enhancing pollination efficiency and/or escape from predator attack, little is known about the degree of these advantages and variations in masting behavior among populations of conspecific plants. METHODS: We determined flowering ramet density and reproductive success (fruit-set success and herbivorous damage) of a perennial herb, Veratrum album subsp. oxysepalum, across six lowland and six alpine populations in northern Japan during 2-3 years. We then analyzed the relationship between floral density and reproductive success to assess the ecological significance of mast flowering. Flowering intervals of individual plants were estimated by counting annual scars on rhizomes. RESULTS: Most populations had mast flowering, but the intervals between flowering for individual plants were shorter in the alpine populations than in the lowland populations. Floral damage by stem borers (dipteran larvae) and seed predation by lepidopteran larvae were intense in the lowland populations. Seed production of individual ramets increased with higher floral density owing to the effective avoidance of floral-stem damage and seed predation. Although stem borers were absent in the alpine habitat, seed predation decreased with higher floral density also in the alpine populations. Pollination success was independent of floral density in both of the alpine and lowland populations. CONCLUSIONS: These results strongly support the predator satiation hypothesis for mast flowering by this species.