Stevia Beverage Consumption prior to Lunch Reduces Appetite and Total Energy Intake without Affecting Glycemia or Attentional Bias to Food Cues: A Double-Blind Randomized Controlled Trial in Healthy Adults.

BACKGROUND: Stevia is a zero-calorie alternative to caloric sugars. Substituting caloric sweeteners with noncaloric sweeteners reduces available energy, but their effects on appetite, subsequent food intake, and neurocognitive responses are still unclear. OBJECTIVE: The aim was to examine whether sweetness with or without calories influences food intake, appetite, blood glucose concentrations, and attentional bias (AB) to food cues. METHODS: This was a randomized, controlled, double-blind crossover study. Healthy participants [n = 20; aged 27 ± 5 y,  55% female; BMI (kg/m2): 21.8 ± 1.5] completed 5 visits, consuming 5 study beverages: 330 mL water (control, no sweet taste, no calories) and either 330 mL water containing 40 g glucose or sucrose (sweet taste; calories, both 160 kcal), maltodextrin (no sweet taste; calories, 160 kcal), or 240 ppm stevia (sweet taste, no calories). Glucose and stevia beverages were matched for sweetness. Subjective appetite ratings and blood glucose were measured at baseline and at 15, 30, and 60 min postprandially. At 15 min participants performed a visual-dot probe task to assess AB to food cues; at 30 min, participants were offered an ad libitum lunch; food intake was measured. RESULTS: Subjective appetite ratings showed that preload sweetness and calorie content both affected appetite. The total AUC for glycemia was significantly higher after the caloric beverages (mean ± SD: maltodextrin, 441 ± 57.6;  glucose, 462 ± 68.1;  sucrose, 425 ± 53.6 mmol × min × L-1 ) compared with both stevia (320 ± 34.2 mmol × min × L-1) and water (304 ± 32.0 mmol × min × L-1) (all P < 0.001). Total energy intake (beverage and meal) was significantly lower after the stevia beverage (727 ± 239 kcal) compared with water (832 ± 198 kcal,  P = 0.013), with no significant difference between the water and caloric beverages (P = 1.00 for water vs. maltodextrin, glucose, and sucrose). However, food-related AB did not differ across conditions (P = 0.140). CONCLUSIONS: This study found a beneficial and specific effect of a stevia beverage consumed prior to a meal on appetite and energy intake in healthy adults. This trial is registered at clinicaltrials.gov as NCT03711084.

Attentional bias to food varies as a function of metabolic state independent of weight status.

Eating behaviour requires that internal metabolic changes are recognized by the central nervous system which regulates brain responses to food cues. This function may be altered in obesity. The aim of this study was to examine potential differences in neurocognitive responses to visual food cues as a function of metabolic state and weight status. A crossover study with two participant groups was conducted, one group with normal-weight (n = 20) and one group with overweight/obesity (n = 22), who completed a novel battery of neurocognitive tests assessing food-cue elicited behavior in both fasted and fed states. The test battery included a visual-dot probe task (VPT), a stimulus-response compatibility task (SRCT) and an implicit association task (IAT). Results from the VPT showed a significant main effect of metabolic state on attentional bias (F(1,40) = 9.90, p = .003, η2p = .198), with participants in the fasted state showing a significantly greater attentional bias for food stimuli than in the fed state. No significant main effect of metabolic state on approach food bias, assessed via the SRCT, or implicit attitudes to food cues, assessed via the IAT, was found and overall, no difference in neurocognitive processing of food cues was demonstrated between participant groups. In the fed state, attentional bias to food cues decreases in both normal-weight controls and participants with overweight/obesity, indicating that changes in current metabolic state can be reflected in attentional processing of visual food cues independently of weight status. Neurocognitive tasks which can effectively and sensitively identify differences in food cue perception according to changes in metabolic status will be useful tools in exploring more complicated interactions between homeostatic and hedonic drives of food intake.

The gut-skin axis in health and disease: A paradigm with therapeutic implications.

As crucial interface organs gut and skin have much in common. Therefore it is unsurprising that several gut pathologies have skin co-morbidities. Nevertheless, the reason for this remains ill explored, and neither mainstream gastroenterology nor dermatology research have systematically investigated the 'gut-skin axis'. Here, in reviewing the field, we propose several mechanistic levels on which gut and skin may interact under physiological and pathological circumstances. We focus on the gut microbiota, with its huge metabolic capacity, and the role of dietary components as potential principle actors along the gut-skin axis. We suggest that metabolites from either the diet or the microbiota are skin accessible. After defining open key questions around the nature of these metabolites, how they are sensed, and which cutaneous changes they can induce, we propose that understanding of these pathways will lead to novel therapeutic strategies based on targeting one organ to improve the health of the other.

Adaptive immunity alters distinct host feeding pathways during nematode induced inflammation, a novel mechanism in parasite expulsion.

Gastrointestinal infection is often associated with hypophagia and weight loss; however, the precise mechanisms governing these responses remain poorly defined. Furthermore, the possibility that alterations in feeding during infection may be beneficial to the host requires further study. We used the nematode Trichinella spiralis, which transiently inhabits the small intestine before migrating to skeletal muscle, as a biphasic model of infection to determine the cellular and molecular pathways controlling feeding during enteric and peripheral inflammation. Through the infection of genetically modified mice lacking cholecystokinin, Tumor necrosis factor α receptors and T and B-cells, we observed a biphasic hypophagic response to infection resulting from two separate immune-driven mechanisms. The enteroendocrine I-cell derived hormone cholecystokinin is an essential mediator of initial hypophagia and is induced by CD4+ T-cells during enteritis. In contrast, the second hypophagic response is extra-intestinal and due to the anorectic effects of TNFα during peripheral infection of the muscle. Moreover, via maintaining naive levels of the adipose secreted hormone leptin throughout infection we demonstrate a novel feedback loop in the immunoendocrine axis. Immune driven I-cell hyperplasia and resultant weight loss leads to a reduction in the inflammatory adipokine leptin, which in turn heightens protective immunity during infection. These results characterize specific immune mediated mechanisms which reduce feeding during intestinal or peripheral inflammation. Importantly, the molecular mediators of each phase are entirely separate. The data also introduce the first evidence that I-cell hyperplasia is an adaptively driven immune response that directly impinges on the outcome to infection.

Mapping glucose-mediated gut-to-brain signalling pathways in humans.

OBJECTIVES: Previous fMRI studies have demonstrated that glucose decreases the hypothalamic BOLD response in humans. However, the mechanisms underlying the CNS response to glucose have not been defined. We recently demonstrated that the slowing of gastric emptying by glucose is dependent on activation of the gut peptide cholecystokinin (CCK1) receptor. Using physiological functional magnetic resonance imaging this study aimed to determine the whole brain response to glucose, and whether CCK plays a central role. EXPERIMENTAL DESIGN: Changes in blood oxygenation level-dependent (BOLD) signal were monitored using fMRI in 12 healthy subjects following intragastric infusion (250ml) of: 1M glucose+predosing with dexloxiglumide (CCK1 receptor antagonist), 1M glucose+placebo, or 0.9% saline (control)+placebo, in a single-blind, randomised fashion. Gallbladder volume, blood glucose, insulin, and GLP-1 and CCK concentrations were determined. Hunger, fullness and nausea scores were also recorded. PRINCIPAL OBSERVATIONS: Intragastric glucose elevated plasma glucose, insulin, and GLP-1, and reduced gall bladder volume (an in vivo assay for CCK secretion). Glucose decreased BOLD signal, relative to saline, in the brainstem and hypothalamus as well as the cerebellum, right occipital cortex, putamen and thalamus. The timing of the BOLD signal decrease was negatively correlated with the rise in blood glucose and insulin levels. The glucose+dex arm highlighted a CCK1-receptor dependent increase in BOLD signal only in the motor cortex. CONCLUSIONS: Glucose induces site-specific differences in BOLD response in the human brain; the brainstem and hypothalamus show a CCK1 receptor-independent reduction which is likely to be mediated by a circulatory effect of glucose and insulin, whereas the motor cortex shows an early dexloxiglumide-reversible increase in signal, suggesting a CCK1 receptor-dependent neural pathway.

Consumption of the Non-Nutritive Sweetener Stevia for 12 Weeks Does Not Alter the Composition of the Human Gut Microbiota.

The use of non-nutritive sweeteners (NNSs) as an alternative to caloric sugars has increased in recent years. Stevia is an NNS that has demonstrated beneficial effects on appetite and energy intake. However, the impact on the gut microbiota is not well understood. Therefore, we investigated how regular consumption of stevia, for up to 12 weeks, impacts the human gut microbiota. Healthy subjects with a normal body mass index participated in our study; the stevia group (n = 14) was asked to consume five drops of stevia twice daily, compared to control participants (n = 13). Faecal samples collected before and after treatment were analysed by 16S rRNA gene sequencing. Stevia did not cause significant changes in the alpha or beta diversity when compared to the control groups. When the relative abundances of taxa were investigated, no clear differences were detected. Conversely, a random forest analysis correctly associated the gut microbiome with the control and stevia groups with an average of 75% accuracy, suggesting that there are intrinsic patterns that could discriminate between control and stevia use. However, large-scale changes in the gut microbiota were not apparent in this study, and, therefore, our data suggest that stevia does not significantly impact the gut microbiota.

Genetic analysis of the Trichuris muris-induced model of colitis reveals QTL overlap and a novel gene cluster for establishing colonic inflammation.

BACKGROUND: Genetic susceptibility to colonic inflammation is poorly defined at the gene level. Although Genome Wide Association studies (GWAS) have identified loci in the human genome which confer susceptibility to Inflammatory Bowel Disease (Crohn's and Ulcerative Colitis), it is not clear if precise loci exist which confer susceptibility to inflammation at specific locations within the gut e.g. small versus large intestine. Susceptibility loci for colitis in particular have been defined in the mouse, although specific candidate genes have not been identified to date. We have previously shown that infection with Trichuris muris (T. muris) induces chronic colitis in susceptible mouse strains with clinical, histological, and immunological homology to human colonic Crohn's disease. We performed an integrative analysis of colitis susceptibility, using an F2 inter-cross of resistant (BALB/c) and susceptible (AKR) mice following T. muris infection. Quantitative Trait Loci (QTL), polymorphic and expression data were analysed alongside in silico workflow analyses to discover novel candidate genes central to the development and biology of chronic colitis. RESULTS: 7 autosomal QTL regions were associated with the establishment of chronic colitis following infection. 144 QTL genes had parental strain SNPs and significant gene expression changes in chronic colitis (expression fold-change ≥ +/-1.4). The T. muris QTL on chromosome 3 (Tm3) mapped to published QTL in 3 unrelated experimental models of colitis and contained 33 significantly transcribed polymorphic genes. Phenotypic pathway analysis, text mining and time-course qPCR replication highlighted several potential cis-QTL candidate genes in colitis susceptibility, including FcgR1, Ptpn22, RORc, and Vav3. CONCLUSION: Genetic susceptibility to induced colonic mucosal inflammation in the mouse is conserved at Tm3 and overlays Cdcs1.1. Genes central to the maintenance of intestinal homeostasis reside within this locus, implicating several candidates in susceptibility to colonic inflammation. Combined methodology incorporating genetic, transcriptional and pathway data allowed identification of biologically relevant candidate genes, with Vav3 newly implicated as a colitis susceptibility gene of functional relevance.

Chronotype in Patients With Immune-Mediated Inflammatory Disease: A Systematic Review.

Immune-mediated inflammatory diseases (IMIDs) such as rheumatoid arthritis, inflammatory bowel disease, and asthma share common pathophysiological pathways characterized by chronic inflammation and subsequent tissue damage involving multiple body sites. Circadian rhythms are 24-h body cycles that regulate immune activity and control the magnitude of immune response based on time of day. Chronotype is a person's individual circadian phase preference, ranging from morningness to eveningness, which is known to influence the risk of cardiometabolic and mental health disease. We systematically reviewed the literature to assess the association of questionnaire-based chronotype and patients with IMID. A comprehensive search of MEDLINE and Embase identified 12 studies meeting the inclusion criteria, conducted in 7 countries and covering 4 IMIDs to include 15,625 IMID patients and 410,783 healthy controls. Results showed that later chronotype may be a risk factor for worse quality of life and increased symptom burden in patients with IMIDs. In addition, chronotype may be a risk factor for IMID incidence, but the direction and magnitude of this effect were not consistent across individual IMIDs. Chronotype assessment could contribute to risk stratification in patients with IMIDs. Cross-disciplinary collaboration to understand the role of circadian rhythms and chronotype in driving common inflammatory pathways could help to improve outcomes for patients with IMIDs.

Malnutrition in systemic sclerosis.

SSc is a chronic multi-system disease with wide-reaching consequences. Gastrointestinal features are present in over 90% of cases and these, together with other disease manifestations, may lead to nutritional decline. This produces substantial morbidity, including reliance on enteral support and even parenteral nutrition-dependent intestinal failure. These complications carry an associated mortality. Up to 18% of patients with SSc are reported to be at high risk of malnutrition [as assessed by Malnutrition Universal Screening Tool (MUST) criteria], with risk increasing with disease severity. Little is known about this decline, its rate of progression and how it affects the individual. Few case series report on nutritional interventions. Most current interventions are based on experience in other diseases. The development of specialist knowledge of SSc-related gastrointestinal disease management and nutritional screening and interventions is required. This paper reviews current knowledge relating to malnutrition and its management in SSc.

Mapping the Homeostatic and Hedonic Brain Responses to Stevia Compared to Caloric Sweeteners and Water: A Double-Blind Randomised Controlled Crossover Trial in Healthy Adults.

Non-nutritive sweeteners have potential effects on brain function. We investigated neural correlates of responses to beverages differing in sweetness and calories. Healthy participants completed 4 randomised sessions: water vs. water with stevia, glucose, or maltodextrin. Blood-oxygenation level-dependent (BOLD) contrast was monitored for 30 min post-ingestion by functional Magnetic Resonance Imaging. A food visual probe task at baseline was repeated at 30 min. A significant interaction of taste-by-calories-by-time was demonstrated mainly in motor, frontal, and insula cortices. Consumption of the stevia-sweetened beverage resulted in greater BOLD decrease, especially in the 20-30 min period, compared to other beverages. There was a significant interaction of taste-by-time in BOLD response in gustatory and reward areas; sweet beverages induced greater reduction in BOLD compared to non-sweet. The interaction calories-by-time showed significantly greater incremental area under the curve in thalamic, visual, frontal, and parietal areas for glucose and maltodextrin 10-20 min post-consumption only, compared to water. In the visual cue task, the water demonstrated an increased response in the visual cortex to food images post-consumption; however, no difference was observed for the three sweet/caloric beverages. In conclusion, both sweet taste and calories exert modulatory effects, but stevia showed a more robust and prolonged effect.

The need to accurately measure energy intake and expenditure in patients with systemic sclerosis.

Background: Malnutrition is common in systemic sclerosis and patients are frequently underweight. However, the balance between assessed dietary energy intake versus expenditure has been neglected to date. This study aimed to assess energy (dietary) intakes and expenditures and to compare discrepancies in systemic sclerosis. Methods: Thirty-six outpatients with systemic sclerosis completed the study. Demographics and clinical data were recorded. Functional questionnaires were completed. Predicted energy requirements were calculated. Over a consecutive 3-day period, patients completed an estimated food diary and wore a specialist energy expenditure monitor (SenseWear® Armband). Assessments of intake and expenditure were compared for individual patients, and the impact according to patient demographics, clinical manifestations and disease severity evaluated. Results: Energy intake did not correlate with predicted (s = 0.117; p = 0.511) or measured (s = -0.039; p = 0.825) expenditures. Predicted and measured energy expenditures correlated, but actual values differed for individuals (intraclass correlation = 0.62; 95% limits of agreement = -459 to 751 kcal). Respiratory involvement was negatively correlated with number of steps (s = -0.350; p = 0.04) and time spent lying (s = 0.333; p = 0.05). There was a significant correlation between body mass index and predicted versus measured energy discrepancy (s = 0.41; p = 0.02), and this discrepancy was greater with higher body mass indices. Conclusion: There was no correlation between intake and either predicted or measured energy expenditure. Predicted and measured energy expenditures were strongly correlated yet differed for the individual patient. In patients with systemic sclerosis, where energy expenditure must be accurately assessed, it should be directly measured.

Appetite, the enteroendocrine system, gastrointestinal disease and obesity.

The enteroendocrine system is located in the gastrointestinal (GI) tract, and makes up the largest endocrine system in the human body. Despite that, its roles and functions remain incompletely understood. Gut regulatory peptides are the main products of enteroendocrine cells, and play an integral role in the digestion and absorption of nutrients through their effect on intestinal secretions and gut motility. Several peptides, such as cholecystokinin, polypeptide YY and glucagon-like peptide-1, have traditionally been reported to suppress appetite following food intake, so-called satiety hormones. In this review, we propose that, in the healthy individual, this system to regulate appetite does not play a dominant role in normal food intake regulation, and that there is insufficient evidence to wholly link postprandial endogenous gut peptides with appetite-related behaviours. Instead, or additionally, top-down, hedonic drive and neurocognitive factors may have more of an impact on food intake. In GI disease however, supraphysiological levels of these hormones may have more of an impact on appetite regulation as well as contributing to other unpleasant abdominal symptoms, potentially as part of an innate response to injury. Further work is required to better understand the mechanisms involved in appetite control and unlock the therapeutic potential offered by the enteroendocrine system in GI disease and obesity.

NIH Workshop Report: sensory nutrition and disease.

In November 2019, the NIH held the "Sensory Nutrition and Disease" workshop to challenge multidisciplinary researchers working at the interface of sensory science, food science, psychology, neuroscience, nutrition, and health sciences to explore how chemosensation influences dietary choice and health. This report summarizes deliberations of the workshop, as well as follow-up discussion in the wake of the current pandemic. Three topics were addressed: A) the need to optimize human chemosensory testing and assessment, B) the plasticity of chemosensory systems, and C) the interplay of chemosensory signals, cognitive signals, dietary intake, and metabolism. Several ways to advance sensory nutrition research emerged from the workshop: 1) refining methods to measure chemosensation in large cohort studies and validating measures that reflect perception of complex chemosensations relevant to dietary choice; 2) characterizing interindividual differences in chemosensory function and how they affect ingestive behaviors, health, and disease risk; 3) defining circuit-level organization and function that link and interact with gustatory, olfactory, homeostatic, visceral, and cognitive systems; and 4) discovering new ligands for chemosensory receptors (e.g., those produced by the microbiome) and cataloging cell types expressing these receptors. Several of these priorities were made more urgent by the current pandemic because infection with sudden acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and the ensuing coronavirus disease of 2019 has direct short- and perhaps long-term effects on flavor perception. There is increasing evidence of functional interactions between the chemosensory and nutritional sciences. Better characterization of this interface is expected to yield insights to promote health, mitigate disease risk, and guide nutrition policy.

Effects of the Daily Consumption of Stevia on Glucose Homeostasis, Body Weight, and Energy Intake: A Randomised Open-Label 12-Week Trial in Healthy Adults.

Stevia is a non-nutritive sweetener, providing sweet taste with no calories. This randomised, controlled, open-label 2-parallel arm trial examined the effects of daily stevia consumption on glycaemia in healthy adults. Secondary endpoints included body weight (BW) and energy intake (EI). Healthy participants (n = 28; aged 25 ± 5y, body mass index 21.2 ± 1.7 kg/m2) were randomised into either the stevia group (n = 14)-required to consume a stevia extract daily-or to the control group (n = 14). At weeks 0 and 12, the glucose and insulin responses to an oral glucose tolerance test were measured; BW and EI were assessed at weeks 0, 6, and 12. There was no significant difference in the glucose or insulin responses. There was a significant main effect of group on BW change (F(1,26) = 5.56, p = 0.026), as the stevia group maintained their weight as opposed to the control group (mean weight change at week 12: -0.22 kg, 95%CI [-0.96, 0.51] stevia group, +0.89 kg, 95%CI [0.16, 1.63] control group). The energy intake was significantly decreased between week 0 and 12 in the stevia group (p = 0.003), however no change was found in the control group (p = 0.973). Although not placebo-controlled, these results suggest that daily stevia consumption does not affect glycaemia in healthy individuals, but could aid in weight maintenance and the moderation of EI.

Randomised clinical trial of a gastrointestinal care bundle to reduce symptoms in patients with pelvic cancer undergoing chemoradiotherapy.

OBJECTIVE: Pelvic radiotherapy is used to treat 17 000 people in the UK each year. Eight in 10 develop difficult bowel problems during pelvic treatment, especially diarrhoea, urgency and incontinence. Some cannot complete treatment, reducing the chance of cancer cure. Undertaking gastroenterologist-led investigation and management during pelvic radiotherapy has never been evaluated. In this study, we aimed to assess whether patients could successfully receive a novel gastrointestinal (GI) care bundle during chemoradiotherapy (feasibility aim) and would experience reduced symptom severity (clinical impact aim). DESIGN: This randomised controlled trial recruited patients with cervical and bladder cancers undergoing radical chemoradiotherapy. Participants were randomised to intervention or control groups. Questionnaire and anthropometric data were collected. All intervention group patients received individualised dietary counselling weekly throughout treatment, and if bowel symptoms developed they were offered rapid-access investigation and treatment for any identified pathology: lactose intolerance, bacterial overgrowth or bile acid malabsorption. RESULTS: Feasibility: 50 participants were recruited, 24 were randomised to the intervention group and 26 to the control group. All completed 20 fractions of external beam pelvic radiotherapy. It was possible to perform 57/72 (79%) of proposed intervention tests with no disruption of oncological management. CLINICAL IMPACT: All participants developed GI symptoms during radiotherapy. The median symptom score for each group increased from baseline at 6 weeks. This was from 0.156 (0.000-0.333) to 0.600 (0.250-1.286) in the control group, and from 0.00 (0.000-0.300) to 0.402 (0.000-0.667) in the intervention group. CONCLUSION: It was feasible to recruit to and deliver a randomised controlled trial of interventions in patients undergoing pelvic chemoradiotherapy. Lower median bowel scores were reported in the intervention group at 6 weeks, with fewer patients experiencing symptoms overall. TRIAL REGISTRATION NUMBER: ISRCTN783488.

Nutritional status and predictors of weight loss in patients with systemic sclerosis.

BACKGROUND & AIMS: Systemic sclerosis (SSc) commonly affects the gastrointestinal (GI) tract and predisposes to malnutrition. Few studies assessed body composition in outpatients with SSc or used more than one method for comparison over time. The aim of this study was to describe markers of nutrition and body composition in patients with SSc and to identify predictors of unintentional weight loss. METHODS: We consecutively included outpatients with SSc and performed a one-year follow-up. Gastrointestinal (GI) involvement was evaluated from clinical investigations. Patients completed questionnaires for organ involvement and functional status. Clinical assessment included body mass index (BMI), the malnutrition universal screening tool (MUST), inter-incisor distance, anthropometry, and bio-electrical impedance analysis (BIA). RESULTS: In total, 168 consecutive patients with SSc were included, and 127 (76%) completed one-year follow-up. Thirteen (8%) died before follow-up. Based on MUST scores, 12% of patients were at high and 14% at medium risk of malnutrition. A low BMI was associated with small intestinal involvement (p < 0.0001). Percentage body fat correlated with BMI, both when using four-site anthropometry (r = 0.65, p < 0.01) and BIA (r = 0.49, p < 0.01). Nine (7%) patients had >5% unintentional weight loss at follow-up. Independent baseline predictors of unintentional weight loss included upper GI involvement and disease severity estimated by Health Assessment Questionnaire Disability Index score. CONCLUSIONS: Nutritional risk and GI involvement are frequent and closely correlated in patients with SSc. BIA and four-site anthropometry are comparable in the clinical assessment of patients with SSc. Unintentional weight loss is discrete and related to disease-specific characteristics.

Sweetness and bitterness taste of meals per se does not mediate gastric emptying in humans.

In cell line and animal models, sweet and bitter tastants induce secretion of signaling peptides (e.g., glucagon-like peptide-1 and cholecystokinin) and slow gastric emptying (GE). Whether human GE and appetite responses are regulated by the sweetness or bitterness per se of ingested food is, however, unknown. We aimed to determine whether intragastric infusion of "equisweet" (Study A) or "equibitter" (Study B) solutions slow GE to the same extent, and whether a glucose solution made sweeter by the addition of saccharin will slow GE more potently than glucose alone. Healthy nonobese subjects were studied in a single-blind, randomized fashion. Subjects received 500-ml intragastric infusions of predetermined equisweet solutions of glucose (560 mosmol/kgH(2)O), fructose (290 mosmol/kgH(2)O), aspartame (200 mg), and saccharin (50 mg); twice as sweet glucose + saccharin, water (volumetric control) (Study A); or equibitter solutions of quinine (0.198 mM), naringin (1 mM), or water (Study B). GE was evaluated using a [(13)C]acetate breath test, and hunger and fullness were scored using visual analog scales. In Study A, equisweet solutions did not empty similarly. Fructose, aspartame, and saccharin did not slow GE compared with water, but glucose did (P < 0.05). There was no additional effect of the sweeter glucose + saccharin solution (P > 0.05, compared with glucose alone). In Study B, neither bitter tastant slowed GE compared with water. None of the solutions modulated perceptions of hunger or fullness. We conclude that, in humans, the presence of sweetness and bitterness taste per se in ingested solutions does not appear to signal to influence GE or appetite perceptions.

Human brain responses to gastrointestinal nutrients and gut hormones.

Functional mapping of human brain activation has made it possible to understand how different nutrients in the gut impact on homeostatic and appetitive brain responses. Current data are limited, but nutrient-specific effects are observed, with differential responses to lipid and sugars. Responses are not a simple function of calorie intake. Gut hormones such as CCK, PYY, GLP-1 and ghrelin are implicated in these responses, but may not exert effects directly on the brain. Research is now addressing how these homeostatic signalling states (fasting/fed) interact with hedonic responses, such as those evoked by images of appealing food. Differences are also beginning to emerge in obese versus lean subjects. These platforms will enable a new understanding of normal and disordered eating behaviours in humans.

Dietary Practices and Beliefs in Patients with Inflammatory Bowel Disease.

BACKGROUND: An epidemiological association implicating diet in IBD risk or protection is widely accepted. Patients with IBD often make links to diet, but there is a dearth of literature exploring dietary perceptions and practices in this population. Our objective was to evaluate dietary beliefs and behaviors in IBD patients. METHODS: We developed a questionnaire assessing demographics, dietary beliefs and habits in IBD patients. This was prospectively administered to 400 consecutive patients attending our IBD clinics. RESULTS: Mean patient age was 48.4 years; 55% were female, 88% white, 39% had Crohn's disease and 51% had ulcerative colitis. Around 48% felt that diet could be the initiating factor in IBD and 57% felt it could trigger a flare. Worsening symptoms with certain foods was reported by 60%. About 66% deprived themselves of their favorite foods in order to prevent relapse. Three-fourth of patients believed that IBD affects appetite, more so during a relapse. Nearly half had never received any formal dietary advice, and two-thirds requested for further dietary advice. After adjusting for other predictors, the IBD subtype and ethnicity of the patients remained as significant factors for influencing beliefs held by patients. CONCLUSIONS: Our study showed that patients hold beliefs pertaining to the role of diet in IBD, with a high level of consistency around key perceived triggers. Whether all the symptoms reported are due to active inflammation cannot be ascertained, but the potential exists for dietary components triggering active disease and perpetuating gut injury, impacting on quality of life and health care costs.