Current Aspects of the Role of Autoantibodies Directed Against Appetite-Regulating Hormones and the Gut Microbiome in Eating Disorders.

The equilibrium and reciprocal actions among appetite-stimulating (orexigenic) and appetite-suppressing (anorexigenic) signals synthesized in the gut, brain, microbiome and adipose tissue (AT), seems to play a pivotal role in the regulation of food intake and feeding behavior, anxiety, and depression. A dysregulation of mechanisms controlling the energy balance may result in eating disorders such as anorexia nervosa (AN) and bulimia nervosa (BN). AN is a psychiatric disease defined by chronic self-induced extreme dietary restriction leading to an extremely low body weight and adiposity. BN is defined as out-of-control binge eating, which is compensated by self-induced vomiting, fasting, or excessive exercise. Certain gut microbiota-related compounds, like bacterial chaperone protein Escherichia coli caseinolytic protease B (ClpB) and food-derived antigens were recently described to trigger the production of autoantibodies cross-reacting with appetite-regulating hormones and neurotransmitters. Gut microbiome may be a potential manipulator for AT and energy homeostasis. Thus, the regulation of appetite, emotion, mood, and nutritional status is also under the control of neuroimmunoendocrine mechanisms by secretion of autoantibodies directed against neuropeptides, neuroactive metabolites, and peptides. In AN and BN, altered cholinergic, dopaminergic, adrenergic, and serotonergic relays may lead to abnormal AT, gut, and brain hormone secretion. The present review summarizes updated knowledge regarding the gut dysbiosis, gut-barrier permeability, short-chain fatty acids (SCFA), fecal microbial transplantation (FMT), blood-brain barrier permeability, and autoantibodies within the ghrelin and melanocortin systems in eating disorders. We expect that the new knowledge may be used for the development of a novel preventive and therapeutic approach for treatment of AN and BN.

Effects of Microbiota Imbalance in Anxiety and Eating Disorders: Probiotics as Novel Therapeutic Approaches.

Anxiety and eating disorders produce a physiological imbalance that triggers alterations in the abundance and composition of gut microbiota. Moreover, the gut-brain axis can be altered by several factors such as diet, lifestyle, infections, and antibiotic treatment. Diet alterations generate gut dysbiosis, which affects immune system responses, inflammation mechanisms, the intestinal permeability, as well as the production of short chain fatty acids and neurotransmitters by gut microbiota, which are essential to the correct function of neurological processes. Recent studies indicated that patients with generalized anxiety or eating disorders (anorexia nervosa, bulimia nervosa, and binge-eating disorders) show a specific profile of gut microbiota, and this imbalance can be partially restored after a single or multi-strain probiotic supplementation. Following the PRISMA methodology, the current review addresses the main microbial signatures observed in patients with generalized anxiety and/or eating disorders as well as the importance of probiotics as a preventive or a therapeutic tool in these pathologies.

A systematic review on the role of microbiota in the pathogenesis and treatment of eating disorders.

BACKGROUND: There is growing interest in new factors contributing to the genesis of eating disorders (EDs). Research recently focused on the study of microbiota. Dysbiosis, associated with a specific genetic susceptibility, may contribute to the development of anorexia nervosa (AN), bulimia nervosa, or binge eating disorder, and several putative mechanisms have already been identified. Diet seems to have an impact not only on modification of the gut microbiota, facilitating dysbiosis, but also on its recovery in patients with EDs. METHODS: This systematic review based on the PICO strategy searching into PubMed, EMBASE, PsychINFO, and Cochrane Library examined the literature on the role of altered microbiota in the pathogenesis and treatment of EDs. RESULTS: Sixteen studies were included, mostly regarding AN. Alpha diversity and short-chain fatty acid (SCFA) levels were lower in patients with AN, and affective symptoms and ED psychopathology seem related to changes in gut microbiota. Microbiota-derived proteins stimulated the autoimmune system, altering neuroendocrine control of mood and satiety in EDs. Microbial richness increased in AN after weight regain on fecal microbiota transplantation. CONCLUSIONS: Microbiota homeostasis seems essential for a healthy communication network between gut and brain. Dysbiosis may promote intestinal inflammation, alter gut permeability, and trigger immune reactions in the hunger/satiety regulation center contributing to the pathophysiological development of EDs. A restored microbial balance may be a possible treatment target for EDs. A better and more in-depth characterization of gut microbiota and gut-brain crosstalk is required. Future studies may deepen the therapeutic and preventive role of microbiota in EDs.

On the origin of eating disorders: altered signaling between gut microbiota, adaptive immunity and the brain melanocortin system regulating feeding behavior.

Research in the field of gut microbiota - brain axis may contribute to clarifying the origin of anorexia nervosa and bulimia, the two principal forms of eating disorders (ED). The initial key findings in ED patients of plasma immunoglobulins (Ig) that react with α-melanocyte-stimulating hormone (α-MSH), a neuropeptide in the brain signaling satiety, have initiated further studies leading to the discovery of the origin of such autoantibodies and to the understanding their possible functional role. An anorexigenic bacterial protein Escherichia coli caseinolytic protease B was recently found to be responsible for the production of α-MSH-cross-reactive autoantibodies and this protein was also detected in human plasma. Another recent study revealed enhanced activation of appetite-regulating the melanocortin type 4 receptor by immune complexes withα-MSH. Taken together, these data serve to build a pathophysiological model of ED presented in this article.

Feeding intolerance alters the gut microbiota of preterm infants.

Feeding intolerance (FI) is a common disease in preterm infants, often causing a delay in individual development. Gut microbiota play an important role in nutrient absorption and metabolism of preterm infants. To date, few studies have focused on the community composition of gut microbiota of preterm infants with feeding intolerance. In this study, we collected fecal samples from 41 preterm infants diagnosed with feeding intolerance and 29 preterm infants without feeding intolerance, at three specific times during the development and prevalence of feeding intolerance (after birth, when feeding intolerance was diagnosed, after feeding intolerance was gone), from different hospitals for 16S rRNA gene sequencing. The gut microbiota community composition of preterm infants diagnosed with feeding intolerance was significantly different from that of preterm infants without feeding intolerance. At the time when feeding intolerance was diagnosed, the relative abundance of Klebsiella in preterm infants with feeding intolerance increased significantly, and was significantly higher than that of the preterm infants without feeding intolerance. After feeding intolerance was cured, the relative abundance of Klebsiella significantly decreased in the infants diagnosed with feeding intolerance, while the relative abundance of Klebsiella in preterm infants without feeding intolerance was not significantly altered during the development and prevalence of feeding intolerance. Furthermore, we verified that Klebsiella was effective in the diagnosis of feeding intolerance (AUC = 1) in preterm infants, suggesting that Klebsiella is a potential diagnostic biomarker for feeding intolerance.

Eating Disorders and the Intestinal Microbiota: Mechanisms of Energy Homeostasis and Behavioral Influence.

PURPOSE OF REVIEW: We reviewed and evaluated recently published scientific studies that explored the role of the intestinal microbiota in eating disorders. RECENT FINDINGS: Studies have demonstrated that the intestinal microbiota is a contributing factor to both host energy homeostasis and behavior-two traits commonly disrupted in patients with eating disorders. To date, intestinal microbiota research in eating disorders has focused solely on anorexia nervosa (AN). Initial studies have reported an atypical intestinal microbial composition in patients with AN compared to healthy controls. However, the impact of these AN-associated microbial communities on host metabolism and behavior remains unknown. The intriguing pattern of findings in patients with AN encourages further investigation of the intestinal microbiota in eating disorders. Elucidating the specific role(s) of these microbial communities may yield novel ideas for augmenting current clinical therapies to promote weight gain, decrease gastrointestinal distress, and even reduce psychological symptomatology.

Feeding Systems and the Gut Microbiome: Gut-Brain Interactions With Relevance to Psychiatric Conditions.

BACKGROUND: Physical and mental health is dependent on the environment, and feeding is a prime example of this environmental exchange. While the hypothalamus controls both feeding behavior and the stress response, the integration of the neural control centers and the peripheral gut allows for disruption in the gastrointestinal systems and dysfunctional communication to the brain. OBJECTIVE: The purpose of this review is to familiarize clinicians with the physiology controlling feeding behavior and its implications for psychiatric conditions, such as anorexia nervosa and depression. Growing understanding of how integrated bacterial life is in the body has shown that gut bacteria regulate basic physiologic processes and are implicated in various disease states and contribute to regulation of mood. Responses to stress have effects on feeding behavior and mood and the regulation of the stress response by the gut microbiota could contribute to the dysfunction seen in patients with psychiatric illnesses. CONCLUSIONS: Gut microbiota may contribute to dysfunction in psychiatric illnesses. New opportunities to modulate existing gut microbiota using probiotics could be novel targets for clinical interventions.

Are the Gut Bacteria Telling Us to Eat or Not to Eat? Reviewing the Role of Gut Microbiota in the Etiology, Disease Progression and Treatment of Eating Disorders.

Traditionally recognized as mental illnesses, eating disorders are increasingly appreciated to be biologically-driven. There is a growing body of literature that implicates a role of the gut microbiota in the etiology and progression of these conditions. Gut bacteria may act on the gut-brain axis to alter appetite control and brain function as part of the genesis of eating disorders. As the illnesses progress, extreme feeding patterns and psychological stress potentially feed back to the gut ecosystem that can further compromise physiological, cognitive, and social functioning. Given the established causality between dysbiosis and metabolic diseases, an altered gut microbial profile is likely to play a role in the co-morbidities of eating disorders with altered immune function, short-chain fatty acid production, and the gut barrier being the key mechanistic links. Understanding the role of the gut ecosystem in the pathophysiology of eating disorders will provide critical insights into improving current treatments and developing novel microbiome-based interventions that will benefit patients with eating disorders.

The Microbiota, the Gut and the Brain in Eating and Alcohol Use Disorders: A 'Ménage à Trois'?

AIMS: Accumulating evidence for the influence of the gut microbiota on the bidirectional communication along the gut-brain axis suggests a role of the gut microbiota in eating disorders (EDs) and alcohol and substance use disorders. The potential influence of altered gut microbiota (dysbiosis) on behaviors associated with such disorders may have implications for developing therapeutic interventions. METHODS: A systematic review of preclinical and clinical studies evaluating the gut microbiota, EDs and alcohol and substance use disorders was conducted using MEDLINE, Embase and Web of Science databases with the objective being to examine the role of the gut microbiota in behavioral correlates of these disorders. Original papers focused on the gut microbiota and potential behavioral implications were deemed eligible for consideration. RESULTS: The resulting 12 publications were limited to gut microbiota studies related to EDs and alcohol and substance use disorders. Some studies suggest that dysbiosis and gut microbial byproducts may influence the pathophysiology of EDs via direct and indirect interference with peptide hormone signaling. Additionally, dysbiosis was shown to be correlated with alcohol use disorder-related symptoms, i.e. craving, depression and anxiety. Finally, a mouse study suggests that manipulations in the gut microbiota may affect cocaine-related behaviors. CONCLUSIONS: Promising, albeit preliminary, findings suggest a potential role of the gut microbiota in behavioral correlates of EDs and alcohol and substance use disorders. SHORT SUMMARY: Preliminary evidence exists supporting the role of the gut microbiota in eating disorders and alcohol and substance use disorders, although additional investigation is needed to determine what is causative versus epiphenomenological.

The Gut-Brain Axis in Healthy Females: Lack of Significant Association between Microbial Composition and Diversity with Psychiatric Measures.

OBJECTIVE: This study examined associations between the composition and diversity of the intestinal microbiota and measures of depression, anxiety, eating disorder psychopathology, stress, and personality in a group of healthy adult females. METHODS: Female participants (n = 91) ages 19-50 years with BMI 18.5-25 kg/m2 were recruited from central North Carolina between July 2014 and March 2015. Participants provided a single fecal sample and completed an online psychiatric questionnaire that included five measures: (i) Beck Anxiety Inventory; (ii) Beck Depression Inventory-II; (iii) Eating Disorder Examination-Questionnaire; (iv) Perceived Stress Scale; and (v) Mini International Personality Item Pool. Bacterial composition and diversity were characterized by Illumina sequencing of the 16S rRNA gene, and associations were examined using Kendall's tau-b correlation coefficient, in conjunction with Benjamini and Hochberg's False Discovery Rate procedure. RESULTS: We found no significant associations between microbial markers of gut composition and diversity and scores on psychiatric measures of anxiety, depression, eating-related thoughts and behaviors, stress, or personality in a large cohort of healthy adult females. DISCUSSION: This study was the first specifically to examine associations between the intestinal microbiota and psychiatric measures in healthy females, and based on 16S rRNA taxonomic abundances and diversity measures, our results do not suggest a strong role for the enteric microbe-gut-brain axis in normal variation on responses to psychiatric measures in this population. However, the role of the intestinal microbiota in the pathophysiology of psychiatric illness may be limited to more severe psychopathology.

Elevated plasma concentrations of bacterial ClpB protein in patients with eating disorders.

OBJECTIVE: Caseinolytic protease B (ClpB) produced by Enterobacteria, such as Escherichia coli, has been identified as a conformational mimetic of α-melanocyte-stimulating hormone (α-MSH), an anorexigenic and anxiogenic neuropeptide. In mice, ClpB induces α-MSH cross-reactive antibodies and activates anorexigenic brain neurons. In patients with eating disorders (ED), anti-ClpB and anti-α-MSH antibodies correlate with psychopathological traits. However, it is not known if ClpB is present in human plasma including ED patients. METHODS: Plasma concentrations of ClpB were measured using a recently developed ClpB immunoassay in female patients with anorexia nervosa, bulimia nervosa, and binge-eating disorder and compared with healthy participants, all characterized by the Eating Disorder Inventory-2 (EDI-2) scale. RESULTS: We found that ClpB was readably detectable in plasma of healthy participants and ED patients and that its concentrations were elevated in ED patients, without significant differences in patient's subgroups. Plasma ClpB concentrations correlated with the EDI-2 scores, with α-MSH as well as with plasma levels of anti-ClpB and anti-α-MSH antibodies. DISCUSSION: These data revealed that bacterial ClpB is naturally present in human plasma and that its concentrations can be elevated in ED patients and associated with ED-related psychopathological traits. These results support a link between bacterial ClpB and the ED pathophysiology. © 2016 Wiley Periodicals, Inc. (Int J Eat Disord 2016; 49:805-808).

Sex-related effects of nutritional supplementation of Escherichia coli: relevance to eating disorders.

OBJECTIVES: The biological background of sex-related differences in the development of eating disorders (EDs) is unknown. Recent data showed that gut bacteria Escherichia coli induce autoantibodies against anorexigenic α-melanocyte-stimulating hormone (α-MSH) associated with psychopathology in ED. The aim of this study was to compare the effects of E. coli on feeding and autoantibodies against α-MSH and adrenocorticotropic hormone (ACTH), between female and male rats. METHODS: Commensal E. coli K12 were given in a culture medium daily to adult Wistar rats by intragastric gavage over a 3-wk period; control rats received culture medium only. RESULTS: Before gavage, E. coli K12 DNA was detected in feces of female but not male rats. E. coli provision was accompanied by an increase in body weight gain in females, but a decrease in body weight gain and food intake in males. Independent of E. coli treatment, plasma levels of anti-α-MSH and ACTH immunoglobulin (Ig)G were higher in female than male rats. Females responded to E. coli by increasing α-MSH IgG levels and affinity, but males by increasing α-MSH IgM levels. Affinity of IgG for ACTH was increased in both E. coli-treated females and males, although with different kinetics. IgG from females stimulated more efficiently α-MSH-induced cyclic adenosine monophosphate production by melanocortin 4 receptor-expressing cells compared with IgG from males. DISCUSSION: Sex-related response to how E. coli affects feeding and anti-melanocortin hormone antibody production may depend on the presence of these bacteria in the gut before E. coli supplementation. These data suggest that sex-related presence of certain gut bacteria may represent a risk factor for ED development.

Effects of eating disorders on oral fungal diversity.

BACKGROUND: The eating disorders anorexia and bulimia nervosa can cause several systemic and oral alterations related to poor nutrition and induced vomiting; however, the oral microflora of these patients is poorly studied. OBJECTIVE: The aim of this study was to evaluate fungal microflora in the oral cavity of these patients by culture-dependent and culture-independent methods. STUDY DESIGN: Oral rinse samples were cultured to assess the prevalence of Candida species, and the isolates were identified by API system. Microorganism counts were compared by the Mann-Whitney test (5%). Ribotyping, a type of molecular analysis, was performed by sequencing the D1/D2 regions of 28S rRNA. RESULTS: Our results demonstrated that the eating disorder group showed higher oral Candida spp. prevalence with culture-dependent methods and higher species diversity with culture-independent methods. CONCLUSIONS: Eating disorders can lead to an increased oral Candida carriage. Culture-independent identification found greater fungal diversity than culture-dependent methods.

The EGFR expression in gastric mucosa of children infected with Helicobacter pylori.

PURPOSE: Epidermal growth factor receptor (EGFR) modulates balance between proliferation and apoptosis in gastric mucosa of the gastrointestinal tract. The aim of the study was to evaluate immunohistochemically the EGFR expression in epithelial and gland cells of antral mucosa in children infected with Helicobacter pylori (H. pylori). MATERIAL/METHODS: The study included 44 children, aged from 5 to 18 years (mean age 13+/-3.4 years) with dyspeptic symptoms, of whom 30 (68.2%) children were infected with H. pylori, 14 (31.8%) children constituted controls. Endoscopic and histopathological assessment of antral mucosa samples was performed according to the Sydney System. Samples taken from gastroscopy were prepared to evaluate EGFR expression in epithelial and gland cells of antrum mucosa according to the manual of a detection kit of EnVision+System-HRP (DAKO). RESULTS: In children H. pylori infected, the EGFR expression in epithelial cells of antral mucosa equaled on average 82.5+/-15 cells/mm2 and ranged from 45.0 to 98.0 cells/mm2 as well as differed statistically significantly when compared to controls (10.2+/-5.0 cells/mm2) (p<0.001). In children with H. pylori infection, the EGFR expression in gland cells of antral mucosa ranged from 2.0 to 85.0 cells/mm2 (mean 25.7+/-22.6 cells/mm2); was lower and differed statistically significantly from controls (54.2 +/- 29.6 cells/mm2) (p<0.001). In children H. pylori infected, there was a statistically significant difference (p<0.001) between the EGFR expression in epithelial and in gland cells of antral mucosa. CONCLUSION: The increased EGFR expression in epithelial cells in comparison with gland cells of antral mucosa in children with H. pylori infection may suggest its role in regeneration processes of gastric mucosa.

Enteropatogenicidad de bacterias aisladas de peces, del agua y plancton de su entorno en Venezuela / Enteropathogenicity of bacteria isolated from fish, water and plancton from their environment in Venezuela

Las enfermedades de transmisión alimentaria asociadas al consumo de pescado, constituyen en la actualidad un grave problema sanitario en Venezuela, ya que la aparición de patologías gastrointestinales se ha hecho cada vez más frecuente, quizás originada directamente por miembros de la bacterioflora de peces dulceacuícolas. En tal sentido, el objetivo de esta investigación se centró en la determinación de la enteropatogenicidad, específicamente la citotoxicidad y enterotoxicidad de cepas bacterianas aisladas de tilapias, truchas arco iris y cachamas, provenientes de granjas y del medio silvestre. Para ello, se emplearon un total de 12 cepas, dos por cada especie bacteriana: Aeromonas hydrophila, Escherichia coli, Klebsiella pneumoniae, Pseudomonas fluorescens, Plesiomonas shigelloides y Vibrio cholerae, empleando la línea celular Vero y a través del modelo de inoculación en ratones lactantes. La producción de enterotoxinas resultó positiva para el 42 por ciento de las cepas, observándose distensión abdominal con fluido intestinal de color blanquecino en ratones inoculados con A. hydrophila, K. pneumoniae y V. cholerae, mientras que en aquellos inoculados con E. coli, el fluido se observó hemorrágico. El 100 por ciento de las cepas resultaron citotóxicas en el ensayo con células Vero, produciendo alteraciones intra (granulaciones tóxicas) y extracelulares (disgregación y cambios en la morfología celular). Estos resultados permiten inferir sobre la existencia de un vínculo entre el consumo de pescado y la aparición de enfermedades en el humano.

Diseases transmitted through food products associated to fish consumption, actually constitute a serious sanitary problem in Venezuela, because gastrointestinal pathologies are more frequent, maybe originated directly from members of freshwater fish bacterioflora. For this, the objective of this research was focused in the enteropathogenicity determination, specifically citotoxicity and enterotoxicity of strains isolated from tilapias, rainbow trouts and cachamas, captured from farms and natural environments. In that sense, 12 strains were used, two of each of the following species: Aeromonas hydrophila, Escherichia coli, Klebsiella pneumoniae, Pseudomonas fluorescens, Plesiomonas shigelloides and Vibrio cholerae, using a Vero cellular line and the suckling mouse model. The enterotoxin production resulted positive for 42 percent of the strains, observing abdominal distension with a whitish intestinal fluid in mice inoculated with Aeromonas hydrophila, Klebsiella pneumoniae and Vibrio cholerae, while in those inoculated with E. coli the fluid was hemorraghic. All the strains resulted citotoxic in the trial with Vero cells, producing intracellular (toxic granulations) and extra cellular alterations (desegregation and changes in the cellular morphology). These results allow the inference that there is a relation between fish consumption and the appearance of disease in humans.

[The prevalence of Microsporidium among adult patients admitted to the parasitology laboratory at the Inonu University Turgut Ozal Medical Center]. / Inönü Universitesi Turgut Ozal Tip Merkezi Parazitoloji Laboratuvarina Gelen Eriskin Hastalarda Microsporidium Görülme Sikligi.

Microsporidium can cause acute and self-restricted diarrhea cases among immunocompetent patients. The aim of this study was to investigate the presence of intestinal parasites and Microsporidium in patients presenting at the internal diseases polyclinic with some digestive system complaints but no immune suppressive problems, and to detect whether it has anything to do with the complaints. A total of 781 fecal samples were investigated for intestinal parasites and Microsporidium. Intestinal parasites were found in 16.11% and Microsporidium in 6.5%. A significant correlation was observed between the presence of intestinal parasites other than Microsporidium and dyspepsia, while in the case of Microsporidium, a significant frequency of dyspepsia and fatigue was observed. It was found that the presence of Microsporidium does not differ by age and gender. From the findings, it was concluded that patients with digestive system complaints should be examined for Microsporidium in addition to intestinal parasites, and the symptoms of dyspepsia and a lack of appetite should especially be given more careful attention.

[Obsessive-compulsive disorders in children. Subtypes of OCD and their relation to infection with group A streptococci]. / Obsessiv-kompulsiv tilstand hos børn. Undertyper af OCD og deres relation til infektion med gruppe-A-beta-haemolytiske streptokokker.

The present review describes the theory of a spectrum of obsessive-compulsive disorders (OCD). This spectrum includes such disorders as trichotillomania, eating disorders, body dysmorphic disorder, and possibly pervasive developmental disorders. OCD with an onset in childhood is presented as a specific subtype, with more boys affected and frequently co-morbid with tics and Tourette's syndrome. Furthermore, it seems to be more genetically determined and have more significant deviations, as measured by neuro-imaging studies, than has OCD with an adult onset. The PANDAS theory (paediatric autoimmune neuropsychiatric disorder associated with streptococcal infections) is described. This subtype of OCD is, still on a speculative basis, connected to infections with beta-haemolytic streptococci. The obsessive-compulsive symptoms are characterised by a sudden onset, "sawtoothed" course with relapses and remissions, and are associated with neurological abnormalities. There are still no clinical consequences in terms of penicillin treatment of this PANDAS subtype of OCD.

A role for Helicobacter pylori in the gastrointestinal complaints of eating disorder patients?

UNLABELLED: Eating disorder patients frequently present with gastrointestinal complaints. Helicobacter pylori is an etiologic factor in type B gastritis, gastric and duodenal ulcers, and may cause nausea and anorexia. OBJECTIVE: To determine whether or not there is an increased prevalence of H. pylori infection in patients with eating disorders. METHOD: Serum H. pylori IgG antibody and gastrointestinal symptoms were assessed in 32 patients admitted for inpatient treatment of anorexia nervosa and/or bulimia nervosa. RESULTS: Eating disorder patients did not have an increased rate of detectable serum H. pylori IgG antibody. DISCUSSION: There is not an increased prevalence of H. pylori infection in eating disorder patients. Thus, the increased frequency of gastrointestinal complaints in eating disorder patients cannot be attributed to H. pylori infection.

Helicobacter pylori infection in adolescents with eating disorders and dyspeptic symptoms.

The potential role of Helicobacter pylori infection of the antrum as a cause of symptoms of dyspepsia in patients with eating disorders was evaluated with an assay to detect H. pylori-specific IgG in serum. H. pylori-specific optical-density readings were comparable for adolescents with eating disorders (0.133 +/- 0.063, mean +/- SD) and for two comparison groups, and were lower than readings for children with documented H. pylori infection. Symptoms referable to the gastrointestinal tract did not correlate with H. pylori status in the teenagers with eating disorders.