Ghrelin is a hormone consisting of 28 amino acids. Growth hormone secretagogue receptor (GHSR) is a receptor for ghrelin, which is expressed in the brain, pituitary gland, and adrenal glands, especially in the hypothalamus. The binding of ghrelin to the receptor 1a subtype mediates most of the biological effects of ghrelin. Ghrelin has a close relationship with the onset of psychosis. Ghrelin can affect the onset of psychosis by regulating neurotransmitters such as dopamine, γ-aminobutyric acid (GABA), and 5-hydroxytryptamine (5-HT) through the hypothalamus-pituitary-adrenal (HPA) axis, brain-gut axis, the mesolimbic dopamine system, and other ways. Ghrelin activates neuropeptide Y (NPY) in the hypothalamic arcuate nucleus (ARC) through the GHSR. Ghrelin binds to neurons in the ventral tegmental area (VTA), where it promotes the activity of dopamine neurons in the nucleus accumbens (NAcs) in a GHSR-dependent way, increasing dopamine levels and the reward system. This article summarized the recent research progress of ghrelin in depression, anxiety, schizophrenia, anorexia nervosa (AN), and bulimia nervosa (BN), and emphasized its potential application for psychiatric disorders treatment.

Gastroparesis is a complex, challenging gastrointestinal disorder presenting with upper gastrointestinal symptoms, especially nausea and vomiting, with significant impact on patients' quality of life. After ruling out mechanical obstruction, it is essential to identify delay in gastric emptying for definitive diagnosis. The most common causes are idiopathic (no identified etiology), diabetes mellitus, and postsurgical status. Management of gastroparesis focuses on dietary modifications and treatment directed to symptom relief. Unfortunately, approximately one-third of patients are refractory to pharmacological therapy, and the effectiveness of the few nonpharmacological options has been questioned.

Extensive review of the literature identifies several uncertainties or controversies regarding the differential diagnosis based on the spectrum of symptoms, the lack of availability of reliable diagnostic test, and questions regarding effective therapeutic options. In this review, we discuss ten controversies regarding gastroparesis: clinical presentation, diagnosis, overlap syndromes, pathophysiology, etiology, as well as pharmacological and nonpharmacological therapeutic options. In addition, we briefly review studies exploring pathological, inflammatory, and molecular disturbances affecting the intrinsic neuromuscular elements that may be involved in the pathophysiology of gastroparesis and may constitute possible therapeutic targets in the future. Finally, we tabulate future research opportunities to resolve these controversies in the management of patients with gastroparesis.

Prior work supports delayed gastric emptying in anorexia nervosa and bulimia nervosa (BN) but not binge-eating disorder, suggesting that neither low body weight nor binge eating fully accounts for slowed gastric motility. Specifying a link between delayed gastric emptying and self-induced vomiting could offer new insights into the pathophysiology of purging disorder (PD).

Women (N = 95) recruited from the community meeting criteria for DSM-5 BN who purged (n = 26), BN with nonpurging compensatory behaviors (n = 18), PD (n = 25), or healthy control women (n = 26) completed assessments of gastric emptying, gut peptides, and subjective responses over the course of a standardized test meal under two conditions administered in a double-blind, crossover sequence: placebo and 10 mg of metoclopramide.

Delayed gastric emptying was associated with purging with no main or moderating effects of binge eating in the placebo condition. Medication eliminated group differences in gastric emptying but did not alter group differences in reported gastrointestinal distress. Exploratory analyses revealed that medication caused increased postprandial PYY release, which predicted elevated gastrointestinal distress.

Delayed gastric emptying demonstrates a specific association with purging behaviors. However, correcting disruptions in gastric emptying may exacerbate disruptions in gut peptide responses specifically linked to the presence of purging after normal amounts of food.

Eating disorders include a spectrum of disordered thinking patterns and behaviours around eating. There is increasing recognition of the bi-directional relationship between eating disorders and gastrointestinal disease. Gastrointestinal symptoms and structural issues might arise from eating disorders, and gastrointestinal disease might be a risk factor for eating disorder development. Cross-sectional research suggests that individuals with eating disorders are disproportionately represented among people seeking care for gastrointestinal symptoms, with avoidant-restrictive food intake disorder in particular garnering attention for high rates among individuals with functional gastrointestinal disorders. This Review aims to describe the research to date on the relationship between gastrointestinal disorders and eating disorders, highlight research gaps, and provide brief, practical guidance for the gastroenterology provider in detecting, potentially preventing, and treating gastrointestinal symptoms in eating disorders.

Individuals with anorexia nervosa (AN) have high levels of gastrointestinal (GI) symptoms, functional GI disorders, and alterations in interoception. The primary aims of the current study were to determine (1) whether individuals with AN differed in gastric physiology as measured by electrogastrography (EGG) as compared to healthy individuals and (2) whether their EGG activity changed from pre- to post-weight restoration.

Adolescent and young adult females receiving inpatient treatment for restricting-type AN (n = 20) and healthy control females (n = 21) completed two EGG sessions, with measurements taken in fasting state and after administration of a water load. Participants with AN completed the first session while underweight and the second session following weight restoration. Healthy control participants also completed two sessions matched for length of time between sessions.

Participants with AN exhibited decreased normogastria post-water load when they were weight restored compared to when they were underweight. Healthy control participants' EGG measures were stable across sessions.

Findings provide evidence for aberrant gastric physiology in individuals with AN who have been weight restored, but not those in the acute phase of the illness. This supports the need for further research on GI functioning in AN.

Anorexia nervosa (AN) is a highly debilitating eating disorder that is difficult to treat. The causes of AN are largely unknown, but some theories suggest problems in gastrointestinal functioning may contribute to the disorder. This study found aberrant gastric functioning in individuals diagnosed with AN after weight restoration treatment. These findings contribute to our understanding of the causes and maintenance of AN and may ultimately lead to better treatments.

Eating disorders (ED) involve both the nervous system and the gastrointestinal tract. A similar double involvement is also found in disorders of the brain-gut interaction (DGBI) and symptoms are sometimes similar.

To find out where there is an association and a cause-effect relationship, we looked for the comorbidity of DGBI and ED.

A systematic review was undertaken. A literature search was performed. Inclusion criteria for the articles retained for analysis were: Observational cohort population-based or hospital-based and case-control studies, examining the relationship between DGBI and ED. Exclusion criteria were: Studies written in other languages than English, abstracts, conference presentations, letters to the Editor and editorials. Selected papers by two independent investigators were critically evaluated and included in this review.

We found 29 articles analyzing the relation between DGBI and ED comprising 13 articles on gastroparesis, 5 articles on functional dyspepsia, 7 articles about functional constipation and 4 articles on irritable bowel syndrome.

There is no evidence for a cause-effect relationship between DGBI and ED. Their common symptomatology requires correct identification and a tailored therapy of each disorder.

Eating disorders involve irregularities in eating behavior that may cause gastrointestinal (GI) symptoms. Consequently, many patients with eating disorders seek gastroenterological healthcare at some point in their illness, with many seeking this care even before they seek treatment for and/or diagnosed with their eating disorder. As such, the gastroenterology provider is in a unique position to identify, manage, and facilitate treatment for an eating disorder early in the course of the illness. Although assessing eating disorders is already a difficult task, the identification of eating disorders in patients with GI disease represents an even greater challenge. In particular, common GI symptoms, such as nausea, vomiting, and bloating, may disguise an eating disorder because these symptoms are often viewed as a sufficient impetus for dietary restriction and subsequent weight loss. In addition, the focus on identifying an organic etiology for the GI symptoms can distract providers from considering an eating disorder. During this prolonged diagnostic evaluation, the eating disorder can progress in severity and become more difficult to treat. Unfortunately, a misconception that hinders eating disorder detection is the notion that the rate or method of weight loss is associated with an eating disorder. Regardless of whether weight loss is slow or rapid, purposeful or accidental, eating disorder behaviors and thought patterns may be present. Unidentified eating disorders are not only dangerous in their own right but also can interfere with effective management of GI disease and its symptoms. As such, it is imperative for the GI provider to remain well versed in the identification of these diseases.

Adult patients with severe chronic small intestinal dysmotility are not uncommon and can be difficult to manage. This guideline gives an outline of how to make the diagnosis. It discusses factors which contribute to or cause a picture of severe chronic intestinal dysmotility (eg, obstruction, functional gastrointestinal disorders, drugs, psychosocial issues and malnutrition). It gives management guidelines for patients with an enteric myopathy or neuropathy including the use of enteral and parenteral nutrition.

Eating disorders (ED) are frequently associated with a wide range of psychiatric or somatic comorbidities. The most relevant ED are anorexia nervosa (AN), bulimia nervosa (BN), and binge eating disorders (BED). Patients with ED exhibit both upper and lower gastrointestinal (GI) symptoms. Evidence of alterations throughout the GI tract in ED will be analyzed given the role of the GI tract in food intake and its regulation. It remains a matter of debate whether GI disorders are inherent manifestations of ED or the results of malnutrition occurring from ED. Moreover, recent clinical studies have highlighted the growing role of intestinal microbiota in the pathogenesis of ED, making it possible to hypothesize a modulation of intestinal microbiota as a co-adjuvant to standard therapy. The aim of this review is to analyze the link between ED and GI diseases and to present, where known, the potential key factors underlying these conditions. Conclusions: The presence of GI disorders should be investigated in patients with ED. Screening for ED should also be encouraged in individuals seeking treatment for unexplained GI complaints to better address therapeutic issues that surround these difficult medical conditions.

Eating disorders (ED) are frequently associated with a wide range of psychiatric or somatic comorbidities. The most relevant ED are anorexia nervosa (AN), bulimia nervosa (BN), and binge eating disorders (BED). Patients with ED exhibit both upper and lower gastrointestinal (GI) symptoms. Evidence of alterations throughout the GI tract in ED will be analyzed given the role of the GI tract in food intake and its regulation. It remains a matter of debate whether GI disorders are inherent manifestations of ED or the results of malnutrition occurring from ED. Moreover, recent clinical studies have highlighted the growing role of intestinal microbiota in the pathogenesis of ED, making it possible to hypothesize a modulation of intestinal microbiota as a co-adjuvant to standard therapy. The aim of this review is to analyze the link between ED and GI diseases and to present, where known, the potential key factors underlying these conditions. Conclusions: The presence of GI disorders should be investigated in patients with ED. Screening for ED should also be encouraged in individuals seeking treatment for unexplained GI complaints to better address therapeutic issues that surround these difficult medical conditions.

Eating disorders, namely anorexia nervosa, bulimia nervosa and binge eating disorder are frequent diseases and often complicated by comorbidities, e.g. psychiatric or cardiovascular comorbidities. It is to note that also gastrointestinal symptoms/complications are frequently observed in patients with eating disorders. These diseases will be presented in the current review along with - where known - possible underlying mechanisms. Lastly, gaps in knowledge will be highlighted.

Postprandial glucose is reduced in malnourished patients with anorexia nervosa (AN), but the mechanisms and duration for this remain unclear. We examined blood glucose, gastric emptying, and glucoregulatory hormone changes in malnourished patients with AN and during 2 wk of acute refeeding compared with healthy controls (HCs). Twenty-two female adolescents with AN and 17 age-matched female HCs were assessed after a 4-h fast. Patients were commenced on a refeeding protocol of 2,400 kcal/day. Gastric emptying (13C-octanoate breath test), glucose absorption (3-O-methylglucose), blood glucose, plasma glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP), insulin, C-peptide, and glucagon responses to a mixed-nutrient test meal were measured on admission and 1 and 2 wk after refeeding. HCs were assessed once. On admission, patients had slower gastric emptying, lower postprandial glucose and insulin, and higher glucagon and GLP-1 than HCs ( P < 0.05). In patients with AN, the rise in glucose (0-30 min) correlated with gastric emptying ( P < 0.05). With refeeding, postprandial glucose and 3-O-methylglucose were higher, gastric emptying faster, and baseline insulin and C-peptide less ( P < 0.05), compared with admission. After 2 wk of refeeding, postprandial glucose remained lower, and glucagon and GLP-1 higher, in patients with AN than HCs ( P < 0.05) without differences in gastric emptying, baseline glucagon, or postprandial insulin. Delayed gastric emptying may underlie reduced postprandial glucose in starved patients with AN; however, postprandial glucose and glucoregulatory hormone changes persist after 2 wk of refeeding despite improved gastric emptying. Future research should explore whether reduced postprandial glucose in AN is related to medical risk by examining associated symptoms alongside continuous glucose monitoring during refeeding.

Individuals with eating disorders, including anorexia nervosa and bulimia nervosa, may present with a range of gastrointestinal (GI) manifestations. The oral cavity, salivary glands, GI tract, pancreas, and liver can be impacted by nutritional restrictive and binge/purging behaviors. Complications are often reversible with appropriate nutritional therapy. At times, however, the complications in these disorders may be severe, irreversible and even life threatening. Given the often covert nature of eating disorders, the practitioner must be attentive to subtle clues that may indicate their presence. Extensive diagnostic evaluations of the GI manifestations of eating disorders should be used only when nutritional rehabilitation does not remedy the problems.

To analyze and compare postoperative morbidity between patients receiving total parenteral nutrition (TPN) and early enteral nutrition supplemented with parenteral nutrition (EEN + PN).

Three hundred and forty patients receiving pancreaticoduodenectomy (PD) from 2009 to 2013 at our center were enrolled retrospectively. Patients were divided into two groups depending on postoperative nutrition support scheme: an EEN + PN group (n = 87) and a TPN group (n = 253). Demographic characteristics, comorbidities, preoperative biochemical parameters, pathological diagnosis, intraoperative information, and postoperative complications of the two groups were analyzed.

The two groups did not differ in demographic characteristics, preoperative comorbidities, preoperative biochemical parameters or pathological findings (P > 0.05 for all). However, patients with EEN + PN following PD had a higher incidence of delayed gastric emptying (16.1% vs 6.7%, P = 0.016), pulmonary infection (10.3% vs 3.6%, P = 0.024), and probably intraperitoneal infection (18.4% vs 10.3%, P = 0.059), which might account for their longer nasogastric tube retention time (9 d vs 5 d, P = 0.006), postoperative hospital stay (25 d vs 20 d, P = 0.055) and higher hospitalization expenses (USD10397 vs USD8663.9, P = 0.008), compared to those with TPN.

Our study suggests that TPN might be safe and sufficient for patient recovery after PD. Postoperative EEN should only be performed scrupulously and selectively.

A systematic review identifying gastrointestinal (GI) complications attributable to anorexia nervosa (AN) was completed.

Studies of any design exploring the pathogenesis of complications and treatment strategies were included. The review was completed in accordance with PRISMA standards.

A total of 123 articles were retained, including one randomized control trial. The majority of included studies were case reports and case series. Controlled studies demonstrated that patients with AN were more likely to have delays in gastric motility, gastric emptying and intestinal transit than comparator groups although results were not uniform across all studies. Published reports suggest that complications can occur at any segment of the GI tract. These issues may derive as a consequence of severe malnourishment, from eating disorder related symptoms such as self-induced purging or from the refeeding process itself. Multiple studies noted that patients with AN report high rates of GI symptoms although in the few cases where medical testing was undertaken, correlations between self-reported symptoms and measurable pathology were not demonstrated.

GI complications may occur throughout the entire GI tract in patients with AN. It is recommended that clinicians use careful judgment when pursuing targeted investigation or introducing symptom specific treatments in response to GI complaints. Evidence suggests that most GI complications resolve with refeeding and cessation of ED symptoms.

The two most clinically serious eating disorders are anorexia nervosa and bulimia nervosa. A drive for thinness and fear of fatness lead patients with anorexia nervosa either to restrict their food intake or binge-eat then purge (through self-induced vomiting and/or laxative abuse) to reduce their body weight to much less than the normal range. A drive for thinness leads patients with bulimia nervosa to binge-eat then purge but fail to reduce their body weight. Patients with eating disorders present with various gastrointestinal disturbances such as postprandial fullness, abdominal distention, abdominal pain, gastric distension, and early satiety, with altered esophageal motility sometimes seen in patients with anorexia nervosa. Other common conditions noted in patients with eating disorders are postprandial distress syndrome, superior mesenteric artery syndrome, irritable bowel syndrome, and functional constipation. Binge eating may cause acute gastric dilatation and gastric perforation, while self-induced vomiting can lead to dental caries, salivary gland enlargement, gastroesophageal reflux disease, and electrolyte imbalance. Laxative abuse can cause dehydration and electrolyte imbalance. Vomiting and/or laxative abuse can cause hypokalemia, which carries a risk of fatal arrhythmia. Careful assessment and intensive treatment of patients with eating disorders is needed because gastrointestinal symptoms/disorders can progress to a critical condition.

Ingestive behaviors in mice are dependent on orosensory cues transmitted via the trigeminal nerve, as confirmed by transection studies. However, these studies cannot differentiate between deficits caused by the loss of the lemniscal pathway vs. the parallel paralemniscal pathway. The paired-like homeodomain protein Prrxl1 is expressed widely in the brain and spinal cord, including the trigeminal system. A knockout of Prrxl1 abolishes somatotopic barrellette patterning in the lemniscal brainstem nucleus, but not in the parallel paralemniscal nucleus. Null animals are significantly smaller than littermates by postnatal day 5, but reach developmental landmarks at appropriate times, and survive to adulthood on liquid diet. A careful analysis of infant and adult ingestive behavior reveals subtle impairments in suckling, increases in time spent feeding and the duration of feeding bouts, feeding during inappropriate times of the day, and difficulties in the mechanics of feeding. During liquid diet feeding, null mice display abnormal behaviors including extensive use of the paws to move food into the mouth, submerging the snout in the diet, changes in licking, and also have difficulty consuming solid chow pellets. We suggest that our Prrxl1(-/-) animal is a valuable model system for examining the genetic assembly and functional role of trigeminal lemniscal circuits in the normal control of eating in mammals and for understanding feeding abnormalities in humans resulting from the abnormal development of these circuits.

Anorexia nervosa is one of a few mental health diagnoses that affects every organ system. Patients with AN often present with multiple secondary effects of starvation at the time of first assessment, including gastrointestinal (GI) complaints. In extreme cases, severe GI complications such as rectal prolapse may be encountered as a consequence of the illness although formal studies investigating the frequency of such occurrences are lacking. We present the case of a 16 year old female previously diagnosed with anorexia nervosa that developed a rectal prolapse as a consequence of her disease as well as a detailed literature review investigating the frequency and prevalence of such occurrences in this population.

To study the prevalence of functional dyspepsia (FD) (Rome III criteria) across eating disorders (ED), obese patients, constitutional thinner and healthy volunteers.

Twenty patients affected by anorexia nervosa, 6 affected by bulimia nervosa, 10 affected by ED not otherwise specified according to diagnostic and statistical manual of mental disorders, 4th edition, nine constitutional thinner subjects and, thirty-two obese patients were recruited from an outpatients clinic devoted to eating behavior disorders. Twenty-two healthy volunteers matched for age and gender were enrolled as healthy controls. All participants underwent a careful clinical examination. Demographic and anthropometric characteristics were obtained from a structured questionnaires. The presence of FD and, its subgroups, epigastric pain syndrome and postprandial distress syndrome (PDS) were diagnosed according to Rome III criteria. The intensity-frequency score of broader dyspeptic symptoms such as early satiety, epigastric fullness, epigastric pain, epigastric burning, epigastric pressure, belching, nausea and vomiting were studied by a standardized questionnaire (0-6). Analysis of variance and post-hoc Sheffè tests were used for comparisons.

90% of patients affected by anorexia nervosa, 83.3% of patients affected by bulimia nervosa, 90% of patients affected by ED not otherwise specified, 55.6% of constitutionally thin subjects and 18.2% healthy volunteers met the Postprandial Distress Syndrome Criteria (χ(2), P < 0.001). Only one bulimic patient met the epigastric pain syndrome diagnosis. Postprandial fullness intensity-frequency score was significantly higher in anorexia nervosa, bulimia nervosa and ED not otherwise specified groups compared to the score calculated in the constitutional thinner group (4.15 ± 2.08 vs 1.44 ± 2.35, P = 0.003; 5.00 ± 2.45 vs 1.44 ± 2.35, P = 0.003; 4.10 ± 2.23 vs 1.44 ± 2.35, P = 0.002, respectively), the obese group (4.15 ± 2.08 vs 0.00 ± 0.00, P < 0.001; 5.00 ± 2.45 vs 0.00 ± 0.00, P < 0.001; 4.10 ± 2.23 vs 0.00 ± 0.00, P < 0.001, respectively) and healthy volunteers (4.15 ± 2.08 vs 0.36 ± 0.79, P < 0.001; 5.00 ± 2.45 vs 0.36 ± 0.79, P < 0.001; 4.10 ± 2.23 vs 0.36 ± 0.79, P < 0.001, respectively). Early satiety intensity-frequency score was prominent in anorectic patients compared to bulimic patients (3.85 ± 2.23 vs 1.17 ± 1.83, P = 0.015), obese patients (3.85 ± 2.23 vs 0.00 ± 0.00, P < 0.001) and healthy volunteers (3.85 ± 2.23 vs 0.05 ± 0.21, P < 0.001). Nausea and epigastric pressure were increased in bulimic and ED not otherwise specified patients. Specifically, nausea intensity-frequency-score was significantly higher in bulimia nervosa and ED not otherwise specified patients compared to anorectic patients (3.17 ± 2.56 vs 0.89 ± 1.66, P = 0.04; 2.70 ± 2.91 vs 0.89 ± 1.66, P = 0.05, respectively), constitutional thinner subjects (3.17 ± 2.56 vs 0.00 ± 0.00, P = 0.004; 2.70 ± 2.91 vs 0.00 ± 0.00, P = 0.005, respectively), obese patients (3.17 ± 2.56 vs 0.00 ± 0.00, P < 0.001; 3.17 ± 2.56 vs 0.00 ± 0.00, P < 0.001 respectively) and, healthy volunteers (3.17 ± 2.56 vs 0.17 ± 0.71, P = 0.002; 3.17 ± 2.56 vs 0.17 ± 0.71, P = 0.001, respectively). Epigastric pressure intensity-frequency score was significantly higher in bulimic and ED not otherwise specified patients compared to constitutional thin subjects (4.67 ± 2.42 vs 1.22 ± 1.72, P = 0.03; 4.20 ± 2.21 vs 1.22 ± 1.72, P = 0.03, respectively), obese patients (4.67 ± 2.42 vs 0.75 ± 1.32, P = 0.001; 4.20 ± 2.21 vs 0.75 ± 1.32, P < 0.001, respectively) and, healthy volunteers (4.67 ± 2.42 vs 0.67 ± 1.46, P = 0.001; 4.20 ± 2.21 vs 0.67 ± 1.46, P = 0.001, respectively). Vomiting was referred in 100% of bulimia nervosa patients, in 20% of ED not otherwise specified patients, in 15% of anorexia nervosa patients, in 22% of constitutional thinner subjects, and, in 5.6% healthy volunteers (χ(2), P < 0.001).

PDS is common in eating disorders. Is it mandatory in outpatient gastroenterological clinics to investigate eating disorders in patients with PDS?

The gastrointestinal tract plays an important role in the improved appetite control and weight loss in response to bariatric surgery. Other strategies which similarly alter gastrointestinal responses to food intake could contribute to successful weight management. The aim of this review is to discuss the effects of surgical, pharmacological and behavioural weight loss interventions on gastrointestinal targets of appetite control, including gastric emptying. Gastrointestinal peptides are also discussed because of their integrative relationship in appetite control. This review shows that different strategies exert diverse effects and there is no consensus on the optimal strategy for manipulating gastric emptying to improve appetite control. Emerging evidence from surgical procedures (e.g. sleeve gastrectomy and Roux-en-Y gastric bypass) suggests a faster emptying rate and earlier delivery of nutrients to the distal small intestine may improve appetite control. Energy restriction slows gastric emptying, while the effect of exercise-induced weight loss on gastric emptying remains to be established. The limited evidence suggests that chronic exercise is associated with faster gastric emptying, which we hypothesize will impact on appetite control and energy balance. Understanding how behavioural weight loss interventions (e.g. diet and exercise) alter gastrointestinal targets of appetite control may be important to improve their success in weight management.

Many studies have reported disturbances of heart rate variability (HRV) in patients with psychosomatic disorders such as anorexia nervosa (AN) and the irritable bowel syndrome (IBS). However, both have never been directly compared.

We compared HRV in AN (n = 21) and in IBS (n = 21) (all females) with 42 healthy female control subjects who were matched for age and in IBS to body mass index (BMI). Recovery periods between different cardiac load tests were compared with baseline recordings and tilt test to estimate time [mean successive difference (MSD)] and frequency domain (Goldberger dimension, frequency of HF peak location and HF power, log HF power) values and to assess general reactivity of the autonomic nervous system (ANS).

Significantly longer inter-beat intervals (IBIs) in AN patients and lower values of MSD in IBS patients were found in comparison with respective controls; both were independent from experimental conditions and are found in baseline recordings only. Both effects were independent of age and BMI. We also demonstrate a significant relationship between age, BMI and some HRV parameters.

Opposite autonomic patterns were found in AN and IBS: stronger vagal withdrawal in IBS and weaker vagal inhibition in AN patients. Records made at rest and without any autonomic load may be representative for assessment of ANS function. Age and BMI should be taken into consideration during assessment of HRV data.

Obesity is recently known as a risk factor for endoscopic gastritis. Adiponectin is an anti-inflammatory cytokine secreted from fat tissue, and its serum concentrations are reduced in obesity. The relation between adiponectin and gastritis remains unclear.

The aim of this study was to determine whether lower serum adiponectin level is associated with the risk of endoscopic gastritis.

We analyzed medical records of participants of a routine health check-up examination. Association among endoscopic findings, serum adiponectin level, and other clinical factors including age, sex, alcohol habit, smoking habit, body mass index (BMI), blood pressure, cholesterol, triglyceride, glucose, and insulin were investigated. Endoscopic erosive gastritis was defined as a flat or minimally depressed white spot surrounded by a reddish area or small elevation with central umbilications mimicking octopus' suckers.

A total of 2,400 participants were enrolled. BMI was significantly higher in gastritis-positive participants than in gastritis-negative participants. Serum adiponectin levels were significantly lower in gastritis-positive participants than in gastritis-negative participants. Multivariate logistic regression analysis revealed that lower serum adiponectin level (OR 0.96; 95% CI 0.93-0.99), smoking (OR 0.50; 95% CI 0.30-0.80), higher blood pressure (OR 1.02; 95% CI 1.01-1.03), and duodenitis (OR 1.8; 95% CI 1.00-3.09) were significantly associated with endoscopic erosive gastritis.

Lower serum level of adiponectin may increase the risk of endoscopic erosive gastritis, independently of BMI. Our findings facilitate further study to clarify the role of hypoadiponectinemia in erosive gastritis.

Functional gastrointestinal disorders (FGIDs) are very common (up to 98%) in patients with an eating disorder (ED). Boyd et al. discuss in this issue of Neurogastroenterology & Motility that FGIDs can persist independently on the outcome of the ED. Their findings leave room for speculation on the mechanisms underlying FGIDs in patients with an ED. FGIDs result from a complex interaction of biological, psychosocial and social factors. The altered eating behavior seen in EDs is strongly associated with disturbed gastrointestinal sensitivity and motor physiology. Moreover, psychiatric co-morbidities in ED patients are also frequently found in FGIDs. The motor and sensitivity disturbances together with psychiatric co-morbidities can lay the foundation of a FGID. Once established the psychological and physiological disturbances can perpetuate and strengthen each other resulting in a FGID that can persist independently of the ED that originally caused the motor and sensitivity disturbances.

Nitric oxide (NO) plays important roles in CNS and smooth muscle function. Here we reveal an additional function in peripheral sensory transmission. We hypothesized that endogenous NO modulates the function of gastrointestinal vagal afferent endings. The nonselective NO synthase (NOS) inhibitor N(G)-nitro-L-arginine methyl ester hydrochloride increased responses to tactile mechanical stimuli of mucosal afferent endings in two species, in some cases severalfold. This was mimicked by a neuronal NOS inhibitor but not an endothelial NOS inhibitor. NOS inhibitors did not affect the responsiveness of smooth muscle afferent endings, suggesting that the endogenous source of NO is exclusively accessible to mucosal receptors. The role of the NO-soluble guanylyl cyclase (sGC)-cGMP pathway was confirmed using the sGC inhibitor 1H-[1,2,4]oxadiazolo[4,3-a]quinoxaline-1-one and the cGMP phosphodiesterase 5' inhibitor sildenafil. The first enhanced and the second inhibited mechanosensory function. Exogenous NO, from the donor S-nitroso-N-acetylpenicillamine, significantly reduced mechanosensitivity of both types of ending. Up to one-third of stomach-projecting afferent neurons in the nodose ganglia expressed neuronal NOS (nNOS). However, anterograde-traced vagal endings were nNOS negative, indicating NOS is not transported peripherally and there are alternative sources of NO for afferent modulation. A subpopulation of enteroendocrine cells in the gut mucosa were nNOS positive, which were found anatomically in close apposition with mucosal vagal afferent endings. These results indicate an inhibitory neuromodulatory role of epithelial NO, which targets a select population of vagal afferents. This interaction is likely to play a role in generation of symptoms and behaviors from the upper gastrointestinal system.

We assessed the impact of a prolonged lipase inhibition upon gastric emptying (GE) and orocecal transit time (OCTT) of a 355-kcal low-fat solid meal.

In double-blind manner, 40 obese women BMI > 30 kg/m2, randomly allocated into two equal groups, took orally t.i.d. 120 mg orlistat or placebo during 8 weeks of a weight-reducing management. At randomization and after 2 months, GE was measured simultaneously with OCTT by means of a 13C-octanoic acid and a hydrogen breath test, respectively. Lipolytic activity was evaluated with a 13C-mixed triglyceride breath test (13C-MTGBT).

A profound lipase inhibition by orlistat was confirmed by a 79.5% +/- 16.9% reduction of the cumulative 6-h 13C recovery with 13CMTGBT. GE remained unchanged either in the orlistat (T1/2, 188 +/- 35 min start versus 198 +/- 36 min end) or the placebo (T1/2, 191 +/- 35 min start versus 180 +/- 39 min end) group. OCTT increased from 208 +/- 54 min to 271 +/- 64 min (P < 0.01) after orlistat treatment and did not change significantly (216 +/- 76 vs. 234 +/- 72 min) in the placebo group.

No adverse effect on the GE and a moderate prolongation of the OCTT of a low-fat solid meal is to be expected under a prolonged treatment with orlistat at a typical dosage regimen.

In previous studies, increasing body mass index (BMI, kg/m(2)) was related to chronic gastrointestinal symptoms, such as frequent vomiting, upper abdominal pain, bloating and diarrhea. However, there have been no reports about the relationship between increasing BMI and abnormal upper endoscopic findings such as gastritis or ulcer.

The study group consisted of 27 319 individuals who underwent medical checkup at a healthcare center from 1 January to 31 December 2003. The following classification of BMI was applied. (i) underweight; BMI < 18.5; (ii) normal weight; 18.5 <or= BMI < 25.0; (iii) overweight; 25.0 <or= BMI < 30.0; and (iv) obese; BMI >or= 30.0. The subjects were grouped according to the findings of upper endoscopy as follows: group 1, those with erosive gastritis, gastric ulcers (benign and malignant) and duodenal ulcers; group 2, those with reflux esophagitis; and group 3, those with findings of upper endoscopy other than group 1 and group 2.

The prevalence of obesity and overweight was 2.2% and 30.5%, respectively. By multivariate analyses, overweight (OR 1.31, 95% CI; 1.22-1.40, P = 0.000) and obesity (OR 1.40, 95% CI; 1.14-1.72, P = 0.001) were significant contributors of group 1. Overweight (OR 1.61, 95% CI; 1.42-1.83, P = 0.000) and obesity (OR 2.23, 95% CI; 1.59-3.11, P = 0.000) were also significant contributors of group 2.

In the general population, increasing BMI was associated with abnormal upper endoscopic findings, such as erosive gastritis, gastric ulcer, duodenal ulcer and reflux esophagitis. Clarification of the cause-and-effect relationships and the mechanisms of these associations require further investigation.

Symptoms of the upper and lower gastrointestinal (gastrointestinal) tract have been described in anorexia nervosa and bulimia nervosa. Studies focusing on general outcome and medical comorbidity describe a worse outcome in the binge eating/purging subtype of anorexia nervosa compared to the restricting subtype. Both anorexia nervosa subtypes experience substantial delays in gastric emptying as well as constipation. These gastrointestinal disturbances may play a role in anorexia nervosa patients' difficulties with refeeding and weight restoration. Bulimia nervosa patients showed increased gastric emptying capacity, with delayed gastric emptying and diminished gastric relaxation. In addition, diminished release of cholecystokinin and abnormalities in enteric autonomic function were found in bulimia nervosa patients. These factors may play a role in the perpetuation of the disease. Gastrointestinal disturbances develop secondary to the disordered eating behaviour and the concomitant malnutrition and subside mostly with the resumption of normal food intake and body weight. Knowledge of these changes may be of critical importance in avoiding misdiagnosis and successful therapy.

Bulimia nervosa (BN) is a psychiatric illness characterized by eating binges followed by inappropriate behavioral attempts to compensate for the binges, usually vomiting or laxative abuse. Patients with BN have disturbances in the development of satiety during a meal as well as disturbances in functions of the upper gastrointestinal tract such as slowed gastric emptying, impaired gastric accommodation reflex and blunted cholecystokinin release. The present study examined gastric compliance and sensory responses to gastric distention in women with BN and controls. Sixteen women with BN and 13 healthy control subjects swallowed an inflatable bag that was placed in the proximal stomach. The bag was inflated to produce increasing steps of pressure against the stomach wall, before and after consumption of a 200 ml (200 Kcal) liquid meal. Pressure and volume were recorded for 2-min periods, beginning at 0 mm Hg pressure and increasing in steps of 2 mm Hg until subjects reported discomfort, gastric volume reached 600 ml, or pressure reached 20 mm Hg. At each pressure step subjects made sensory ratings. Gastric compliance was calculated as the slope of the best-fit straight line of each subject's gastric volume vs. gastric pressure. There was a significant postmeal increase in gastric compliance in both groups of subjects but there was no difference in compliance between patients with BN and controls. Patients with BN appeared to have diminished sensitivity to gastric distention. In conclusion, although other studies have described gastrointestinal abnormalities associated with BN, the current study found gastric compliance of patients with BN to be normal.

Gastric emptying is frequently delayed in critical illness which compromises the success of nasogastric nutrition. The underlying motor dysfunctions are poorly defined.

To characterise antro-pyloro-duodenal motility during fasting, and in response to gastric and duodenal nutrient, as well as to evaluate the relationship between gastric emptying and motility, in the critically ill.

Fifteen mechanically ventilated patients from a mixed intensive care unit; 10 healthy volunteers.

Antro-pyloro-duodenal pressures were recorded during fasting, after intragastric administration (100 ml; 100 kcal), and during small intestinal infusion of liquid nutrient (6 hours; 1 kcal/min). Gastric emptying was measured using a (13)C octanoate breath test.

In healthy subjects, neither gastric nor small intestinal nutrient affected antro-pyloro-duodenal pressures. In patients, duodenal nutrient infusion reduced antral activity compared with both fasting and healthy subjects (0.03 (0-2.47) waves/min v 0.14 (0-2.2) fasting (p = 0.016); and v 0.33 (0-2.57)/min in healthy subjects (p = 0.005)). Basal pyloric pressure and the frequency of phasic pyloric pressure waves were increased in patients during duodenal nutrient infusion (3.12 (1.06) mm Hg; 0.98 (0.13)/min) compared with healthy subjects (-0.44 (1.25) mm Hg; p<0.02 after 120 minutes; 0.29 (0.15)/min; p = 0.0002) and with fasting (-0.06 (1.05) mm Hg; p<0.03 after 160 minutes; 0.49 (0.13)/min; (p = 0.0001). Gastric emptying was delayed in patients (gastric emptying coefficient 2.99 (0.2) v 3.47 (0.1); p = 0.015) and inversely related to the number of pyloric pressure waves (r = -0.563, p = 0.029).

Stimulation of pyloric and suppression of antral pressures by duodenal nutrient are enhanced in the critically ill and related to decreased gastric emptying.

To investigate energy expenditure and glucose metabolism after a standard oral glucose load (75 g) in 8 normal weight bulimic women and 8 normal weight control women and to evaluate the relative endocrine implication.

Serum glucose and insulin were measured both in basal conditions and after the glucose load; a basal endocrine assessment and body composition was evaluated and glucose induced thermogenesis (GIT) was calculated during 300 min following the glucose load.

Serum glucose levels were significantly lower in bulimics both in fasting and in post-prandial state. Insulin levels were similar in bulimic and control women before and after the glucose load. FSH, leptin and free urinary cortisol (FUC) were all within the normal ranges, but significantly lower in bulimic patients compared with controls (p < 0.001). Fat mass (FM) and Fat-free mass (FFM) were reduced in bulimic patients, even if they normalized after correction per body weight. Resting energy expenditure (REE) was similar in the two groups even after FFM normalization, while GIT was lower in bulimic patients and it was strongly related to free urinary chortisol. Glucose oxidation was higher in fasting state and post glucose load, while lipid oxidation was strongly reduced.

An energy preservation mechanism seems to be the key element for normal-weight bulimic patients' metabolism, consisting in leptin levels and GIT reduction, and lipid oxidation inhibition.

Anorexia nervosa (AN) and bulimia nervosa (BN) are disorders of eating and weight-related behavior that together afflict some 1-3% of women in the United States. One of the remarkable features about each of the eating disorders is how persistent the disordered eating behavior becomes once it has begun. Substantial psychological, social, and physiological disturbances are associated with eating disorders, and it has been very difficult to disentangle those factors that may result from the disturbed behavior from the factors that may have predisposed individuals to, or precipitated the development of, the disorder. This article will briefly review the definitions, phenomenology, and identified risk factors for development of each of the major eating disorders. Pathophysiology will be discussed, with a particular focus on candidate factors that might sustain disordered eating behavior, as informed by clinical and basic science research. Future research directions will be suggested.

An unexplained epidemic of obesity is occurring but the relationship between obesity and gastrointestinal (GI) tract function is unclear. We aimed to evaluate the association between body mass index (BMI) and specific GI symptoms.

A birth cohort in Dunedin, New Zealand, aged 26 yr (n = 980, 94% of total original sample) was evaluated using a validated GI symptom questionnaire. Categories of GI symptom complexes were defined a priori. The association of reported GI symptoms with BMI (kg/m(2)) was assessed adjusting for gender.

The prevalence of obesity (BMI > or = 30 kg/m(2)) was 12%; 30% were overweight. There was a significant univariate positive association between increased BMI and diarrhea (>3 stools/day, loose stools, or urgency); the sex adjusted odds ratio for obese versus normal weight was 1.8 (95% CI 1.1, 2.9; p= 0.02). Abdominal pain associated with nausea or vomiting was positively associated with increased BMI (OR 2.0, 95% CI 1.0, 2.9; p= 0.04). Being overweight was negatively associated with abdominal pain and constipation (OR 0.4, 95% CI 0.2, 0.9; p= 0.02). Irritable bowel syndrome and reflux symptoms were not significantly associated with increased BMI. Waist-to-hip ratios were not significantly associated with GI symptoms. No study members were taking antiobesity medications. Hemoglobin A1c levels were not associated with any of the GI symptoms.

In a general population sample of young adults, increasing BMI was associated with diarrhea and abdominal pain with nausea/vomiting.

Perception of sensations arising from the gastrointestinal tract may be diminished in obese subjects and thus facilitate overeating. Alternatively, excess food intake may cause gastrointestinal (GI) symptoms in obese patients. We evaluated the relationship between body mass index (BMI) and specific GI symptoms in the community.

Residents of Olmsted County, MN were selected at random to receive by mail one of two validated questionnaires. The association of reported GI symptoms with BMI (kg/m(2)) was assessed using a logistic regression analysis adjusting for age, gender, psychosomatic symptom score, and alcohol and tobacco use.

Response rate was 74% (1,963 of 2,660). The prevalence of obesity (BMI > or = 30 kg/m(2)) was 23%. There was a positive relationship between BMI and frequent vomiting (p= 0.02), upper abdominal pain (p= 0.03), bloating (p= 0.002), and diarrhea (p= 0.01). The prevalence of frequent lower abdominal pain, nausea, and constipation was increased among obese (BMI > or = 30 kg/m(2)) compared to normal weight participants, however, no significant association was found between BMI and these symptoms.

In the community, increasing BMI is associated with increased upper GI symptoms, bloating, and diarrhea. Clarification of the cause-and-effect relationships and the mechanisms of these associations require further investigation.

Gastrointestinal symptoms are common in anorexia and in bulimia nervosa, but their relationship with gastric dysmotility and their possible improvement with refeeding are still debated.

Twenty-three anorexic patients (12 with the binge/purging and 11 with the restricting subtypes) were studied using an ultrasonographic gastric-emptying test, psychopathological questionnaires, and bowel symptom questionnaires, before and after 4 and 22 wk rehabilitation.

Gastric symptom scores were markedly higher in patients than in controls and improved significantly with treatment. On entry, compared to controls, gastric emptying was significantly delayed in restricters and purgers (357 +/- 25.3 and 360 +/- 13.0 min, respectively, mean +/- SEM; controls 207 +/- 9.1). After 4 and 22 wk of treatment, it improved in restricters (315 +/- 20.1 and 296 +/- 17.2 min, respectively), but not in purgers (337 +/- 14.3 and 335 +/- 15.9 min). No relationship was found between entry values of symptoms of gastric emptying and of psychopathological tests or between their variations over time.

Gastric emptying derangement and dyspeptic symptoms are present in both subtypes of anorexia nervosa patients. Long-term rehabilitation improves gastrointestinal symptoms, gastric emptying, and psychopathological distress in an independent manner, whereas short-term refeeding does not.

Because the stomach plays an important role in the development of satiety, gastric function was examined in bulimia nervosa (BN).

Sixteen patients with BN and 16 controls swallowed an inflatable bag, which was positioned in the proximal stomach. Minimal distending pressure (MDP), the pressure needed to overcome intraabdominal pressure, was determined. Gastric volume was recorded after subjects drank a liquid meal.

MDP was similar in patient and control groups (7.56 +/- 2.13 vs. 7.13 +/- 2.06 mmHg; t =.57, df = 30, p =.58). Average postmeal gastric relaxation was significantly lower in the patient group (29.7 +/- 97.8 vs. 105.1 +/- 103.3 mL; t = 2.13, df = 30, p =.042).

Stomach relaxation following food consumption is significantly diminished in patients with BN. Physiologic abnormalities of stomach function in BN may contribute to the perpetuation of disturbances in behavior in this disorder.

Patients with eating disorders can refer to a variety of gastrointestinal symptoms, sometimes to justify reduced food intake and vomiting. The authors investigated whether adolescent patients with eating disorders and dyspeptic symptoms have altered gastric electric activity and abnormal gastric emptying as assessed respectively by electrogastrography and scintigraphy.

Twenty-eight patients (18 with anorexia and 10 with bulimia) and 16 healthy volunteers underwent electrogastrography; 20 of the 28 patients (14 with anorexia and 6 with bulimia) underwent gastric emptying scintigraphy. Electrogastrography with bipolar recording lasted 1 hour, 30 minutes before and after a standard meal. Before gastric emptying scintigraphy, patients fasted overnight; during testing, they ingested a solid meal labeled with technetium-99m sulfur colloid. The ratio of fasting to postprandial electrogastrographic variables was evaluated using the Wilcoxon matched-pair test. The Mann- Whitney test was used to compare absolute values for electrogastrographic data in each group. The Student paired t test was used to compare scintigraphic results expressed as percentage of gastric emptying at 60 minutes and as the gastric emptying time (T(1/2)).

Patients with bulimia significantly differed from those with anorexia and control subjects regarding the amount of normal gastric electric activity and bradygastria, and from patients with anorexia only regarding tachygastria. These electrogastrographic variables did not differ significantly between patients with anorexia and control subjects. Gastric emptying time (T(1/2)) was significantly longer in patients with bulimia than in those with anorexia.

Adolescent patients with bulimia who complain of dyspeptic symptoms have documentable abnormalities of gastric electric activity and emptying, whereas their counterparts with anorexia, probably owing to their shorter disease duration, do not.

The correlates of specific childhood feeding problems are described to further examine possible predisposing factors for feeding problems. We report our experience with 349 participants evaluated by an interdisciplinary feeding team.

A review of records was conducted and each participant was identified as having one or more of five functionally defined feeding problems: food refusal, food selectivity by type, food selectivity by texture, oral motor delays, or dysphagia. The prevalence of predisposing factors for these feeding problems was examined. Predisposing factors included developmental disabilities, gastrointestinal problems, cardiopulmonary problems, neurological problems, renal disease and anatomical anomalies.

The frequencies of predisposing factors varied by feeding problem. Differences were found in the prevalence of the five feeding problems among children with three different developmental disabilities: autism, Down syndrome and cerebral palsy. Gastro-oesophageal reflux was the most prevalent condition found among all children in the sample and was the factor most often associated with food refusal. Neurological conditions and anatomical anomalies were highly associated with skill deficits, such as oral motor delays and dysphagia.

Specific medical conditions and developmental disabilities are often associated with certain feeding problems. Information concerning predisposing factors of feeding problems can help providers employ appropriate primary, secondary and tertiary prevention measures to decrease the frequency or severity of some feeding problems.

Gastric emptying may be delayed in HIV infection. We aimed to characterize the pattern of gastric emptying in HIV seropositive subjects and correlate the findings with symptoms, as well as to identify possible etiological factors. Solid gastric emptying was measured using scintigraphy in 54 HIV seropositive subjects and 12 HIV seronegative controls. Gastrointestinal symptoms were evaluated using a standardized numerical score, and autonomic function was assessed using spectral analysis of heart rate variability. Fasting and postprandial duodenojejunal activity was recorded using strain gauge manometry catheters. Gastric emptying rate, but not lag phase, was significantly delayed in HIV-infected subjects, particularly those with enteric infections and more advanced disease. Delayed gastric emptying did not correlate with symptoms, autonomic dysfunction, or small intestinal motility. In conclusion, abnormalities found in autonomic function and gastric emptying in HIV infection are multifactorial in nature. The contribution of upper gastrointestinal motor dysfunction to gastric symptoms in such individuals is unclear.

Gastric emptying can be modified by different physiologic conditions such as aging, menstrual cycle and pregnancy. Few studies in the literature have compared the gastric emptying rate of solid meals in normal subjects of varying size. The purpose of this work is to evaluate the gastric emptying rate of solid meals to determine whether body mass index (BMI) and gastric emptying rate correlate. Both ultrasonographic and scintigraphic techniques have been employed. Twenty-four healthy male subjects, divided into two groups, participated in the study. Our results demonstrate a significant correlation between gastric emptying and BMI. We conclude that variability of BMI must be taken in account when measurements of gastric emptying of solid food are performed.

The effects of different macronutrients on appetite and pyloric motility and the impact of short-term dietary glucose supplementation on these responses were evaluated. Ten males (aged 19-38 yr) received isocaloric (2.9 kcal/min) intraduodenal infusions of glucose and lipid while antropyloroduodenal motility and appetite were assessed by manometry and visual analog scales, respectively. Effects of each intraduodenal nutrient on appetite and motility were evaluated before and after 7 days of dietary supplementation with glucose (400 g daily). Initially, both nutrients caused a similar rise in pyloric tone, but intraduodenal lipid was a more potent stimulus of phasic pyloric motility (P = 0.05) and suppressed appetite more (P = 0.013) than intraduodenal glucose. After dietary glucose supplementation, the increase in pyloric tone during intraduodenal glucose was attenuated. Although intraduodenal lipid remained a more potent stimulant of phasic pyloric motility (P = 0.016), it no longer decreased appetite. We conclude that in healthy young males 1) intraduodenal infusion of lipid is a more potent stimulus of phasic pyloric motility and suppresses appetite more than intraduodenal glucose and 2) dietary glucose supplementation alters both the appetite suppressant effect of intraduodenal lipid and the pyloric motor response to intraduodenal glucose infusion.

Bulimia nervosa remains a common eating disorder in young women. Little is known about upper gastrointestinal symptoms or gastric motility in patients with bulimia nervosa. The aim of this study was to measure gastric myoelectrical activity and hunger/satiety and stomach emptiness/fullness before and after a non-nutrient water load and solid-phase gastric emptying in hospitalized patients with bulimia nervosa (n = 12) and in healthy women (n = 13). Gastric myoelectrical activity was measured by means of cutaneous electrodes; visual analogue scales were used to measure perceptions of hunger/satiety and stomach emptiness/fullness. Before and after a standard water load the bulimia patients reported significantly greater stomach fullness and satiety compared with control subjects (P < 0.01). The percentage of gastric myoelectrical power in the normal 3 cpm range was significantly less in bulimics compared with controls. Power in the 1-2 cpm bradygastria range was significantly greater in bulimia patients before and after the water load compared with the control subjects (P < 0.05). Solid-phase gastric emptying studies using radio-isotope-labelled scrambled eggs showed the lag phase was shortened in the bulimic patients (16 +/- 4 min vs 31 +/- 4 min in controls, P < 0.01), but the percentage of meal emptied at 2 h was similar to control values.

bulimia patients had exaggerated perceptions of stomach fullness and satiety in response to water; and abnormal gastric myoelectrical activity and accelerated lag phase of gastric emptying were objective stomach abnormalities detected in hospitalized patients with bulimia nervosa.

The high energy requirements in cystic fibrosis (CF) increase the likelihood of malnutrition. Delayed mouth-to-cecum transit times have been reported and raise the possibility that abnormalities of gastric function in CF contribute to reduced food intake. The aims of this project were to document solid-phase gastric emptying times in young people with CF and age- and sex-matched healthy controls, and to investigate whether delayed gastric emptying contributes to suboptimal energy intakes.

Nineteen subjects with CF, mean age 12.6 years (11 girls and 8 boys), and 17 control subjects, mean age 12.8 years (9 girls and 8 boys), were studied. Energy intake was assessed by means of a 4-day weighed food record. Fecal fat excretion was determined from a 3-day stool collection. Gastric emptying was assessed with a standard test meal of pancakes labeled with 99mTc-macroalbumin aggregates. The half emptying time of solids from the stomach was recorded.

The mean solid-phase gastric emptying time was significantly faster in the CF subjects compared with normal, healthy, age- and sex-matched control subjects (53 min vs. 72.2 min, p < 0.05). Energy intakes, measured as the percentage of the recommended energy intake for age and sex, were greater in the CF subjects than in the control subjects (115% vs. 89%, p < 0.01), whereas the mean % FFE for the CF subjects was 9.9%. CF subjects with longer gastric emptying times also had lower relative energy intakes (r = -0.50, p < 0.05).

Gastric emptying time in healthy subjects with CF is rapid. Faster solid-phase gastric emptying times may be secondary to high-fat, high-energy intakes and may represent a survival advantage.

Young women report symptoms associated with irritable bowel syndrome (IBS), such as pain, bloating, and changes in bowel movements, more often than young men. Young women with eating disorders also report these gastrointestinal symptoms frequently. We hypothesized that if dieting behaviors were associated with these symptoms, the prevalence and frequency of the symptoms would be positively related to dieting severity in young women. We interviewed 301 1st-year college women representing the continuum of dieting severity. We found that severity of dieting was positively related to frequency of abdominal pain, bloating, diarrhea, and constipation, and that the women who reported 3 or more symptoms regularly scored higher on a scale for dieting severity. Although this study did not examine the relationship between dieting severity and clinical IBS, the findings suggested that dieting is associated with gastrointestinal symptoms in young women.

Recent observations indicate that gastric emptying may be influenced by patterns of previous nutrient intake. The aims of this study were to determine the effects of a high glucose diet on gastric emptying of glucose and fructose, and the impact of any changes in gastric emptying on plasma concentrations of glucose, insulin and gastric inhibitory polypeptide in response to glucose and fructose loads. Gastric emptying of glucose and fructose (both 75 g dissolved in 350 ml water) were measured in seven normal volunteers on separate days while each was on a "standard' diet and an identical diet supplemented with 440 g/day of glucose for 4-7 days. Venous blood samples for measurement of plasma glucose, insulin and gastric inhibitory polypeptide levels were taken immediately before and for 180 min after ingestion of glucose and fructose loads. Dietary glucose supplementation accelerated gastric emptying of glucose (50% emptying time 82 +/- 8 vs 106 +/- 10 min, p = 0.004) and fructose (73 +/- 9 vs 106 +/- 9 min, p = 0.001). After ingestion of glucose, plasma concentrations of insulin (p < 0.05) and gastric inhibitory polypeptide (p < 0.05) were higher during the glucose-supplemented diet. In contrast, plasma glucose concentrations at 60 min and 75 min were lower (p < 0.05) on the glucose-supplemented diet. We conclude that short-term supplementation of the diet with glucose accelerates gastric emptying of glucose and fructose, presumably as a result of reduced feedback inhibition of gastric emptying from small intestinal luminal receptors. More rapid gastric emptying of glucose has a significant impact on glucose tolerance.