The study of the intestinal or gut microbiome is a newer field that is rapidly gaining attention. Bidirectional communication between gut microbes and the host can impact numerous biological systems regulating immunity and metabolism to either promote or negatively impact the host’s health. Habitual routines, dietary choices, socioeconomic status, education, host genetics, medical care and environmental factors can all contribute to the composition of an individual’s microbiome. A key environmental factor that may cause negative outcomes is the consumption of nicotine products. The effects of nicotine on the host can be exacerbated by poor dietary choices and together can impact the composition of the gut microbiota to promote the development of metabolic disease including non-alcoholic fatty liver disease. This review explores the contribution of nicotine, poor dietary choices and other unhealthy lifestyle factors to gut dysbiosis.
Pediatric gastroenterology is the only pediatric subspecialty with nutrition as part of its official curriculum and objective. However, pediatric gastroenterology fellows feel that their baseline knowledge in nutrition is suboptimal. The purpose of this study was to assess the perceived effectiveness of nutrition training among pediatric gastroenterologists, identify areas of need for additional education, and determine the perceived role of the gastroenterologist in obesity management. Methods A survey was sent to members and fellows of the North American Society of Pediatric Gastroenterology, Hepatology and Nutrition (NASPGHAN) to assess general nutrition education as well as obesity management and educational needs. Results A total of 272 responses were received, for an overall response rate of 15.2% (272/1,784). Most responders reported having average or above-average knowledge base in all nutritional topics. There was strong interest in additional resources and a continuing medical education (CME) module on several nutrition topics including: nutritional requirements in specific gastrointestinal (GI) disease, failure to thrive/growth failure, and parenteral nutrition support, with the format of CME dependent on the topic. There was also a strong interest in additional CME on the management of pediatric obesity (67%), as most responders felt that the management of obesity in children requires subspecialty care. However, the perceived role of the pediatric gastroenterologist was one of support to treat the gastrointestinal and hepatic co-morbidities of obesity rather than serve as the main provider of comprehensive obesity care. Conclusion Pediatric gastroenterologists identified gaps in their nutrition knowledge base that may be attributed to the current nutrition education training during fellowship. Multiple topics were identified for additional nutrition education, including obesity management. The nutrition management challenges of today necessitate improved baseline nutrition knowledge and this focus on nutrition should begin at the fellowship level.
A generalized absence of enteroendocrine cells characterizes 2 diarrheal/malabsorptive diseases, namely, enteroendocrine cell dysgenesis and autoimmune polyglandular syndrome 1. However, it is not routine for pathologists to examine mucosal biopsies for enteroendocrine cells in cases of chronic diarrheal illness. Our primary aim was to prospectively examine colonic mucosa for loss of enteroendocrine cells using chromogranin A immunohistochemistry for diagnostic purposes. Our secondary aim was to investigate enterochromaffin cells as a subset of enteroendocrine cells, using serotonin (5HT) immunohistochemistry; we hypothesized that other causes of diarrhea due to loss of enteroendocrine cell subsets are missed by evaluating enteroendocrine cells alone. Our approach was limited to patients with chronic unexplained diarrhea partly selected by referring physicians who considered the patients problematic. Seven problematic patients with reduced enteroendocrine or enterochromaffin cells were collected over a 9-month period and placed in group A. Three group A patients demonstrated reduced enteroendocrine cells relative to controls, and they were later diagnosed as having enteroendocrine cell dysgenesis (n = 1) and autoimmune polyglandular syndrome 1 (n = 2). Four group A patients had reduced enterochromaffin cells but normal enteroendocrine cells. These 4 patients had conditions such as congenital diarrhea, mild graft-versus-host disease, acquired childhood chronic diarrhea, and diarrhea post lung transplant. The reduced enterochromaffin cells in the graft-versus-host disease patient inspired a third aim, that is, to investigate whether a loss of enterochromaffin cells would be a generalized defect seen in patients with mild colonic graft-versus-host disease (group B). However, no loss of enterochromaffin cells was detected in group B. Two methods of enumerating endocrine cells were used and demonstrated 67% agreement.
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