Digestion and Absorption Use of Physico-Chemical Concepts and Techniques
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Coffee and Its Effect on Digestion
Expert report Coffee and its effect on digestion By Dr. Carlo La Vecchia, Professor of Medical Statistics and Epidemiology, Dept. of Clinical Sciences and Community Health, Università degli Studi di Milano, Italy. Contents 1 Overview 2 2 Coffee, a diet staple for millions 3 3 What effect can coffee have on the stomach? 4 4 Can coffee trigger heartburn or GORD? 5 5 Is coffee associated with the development of gastric or duodenal ulcers? 6 6 Can coffee help gallbladder or pancreatic function? 7 7 Does coffee consumption have an impact on the lower digestive tract? 8 8 Coffee and gut microbiota — an emerging area of research 9 9 About ISIC 10 10 References 11 www.coffeeandhealth.org May 2020 1 Expert report Coffee and its effect on digestion Overview There have been a number of studies published on coffee and its effect on different areas of digestion; some reporting favourable effects, while other studies report fewer positive effects. This report provides an overview of this body of research, highlighting a number of interesting findings that have emerged to date. Digestion is the breakdown of food and drink, which occurs through the synchronised function of several organs. It is coordinated by the nervous system and a number of different hormones, and can be impacted by a number of external factors. Coffee has been suggested as a trigger for some common digestive complaints from stomach ache and heartburn, through to bowel problems. Research suggests that coffee consumption can stimulate gastric, bile and pancreatic secretions, all of which play important roles in the overall process of digestion1–6. -
The Oesophagus Lined with Gastric Mucous Membrane by P
Thorax: first published as 10.1136/thx.8.2.87 on 1 June 1953. Downloaded from Thorax (1953), 8, 87. THE OESOPHAGUS LINED WITH GASTRIC MUCOUS MEMBRANE BY P. R. ALLISON AND A. S. JOHNSTONE Leeds (RECEIVED FOR PUBLICATION FEBRUARY 26, 1953) Peptic oesophagitis and peptic ulceration of the likely to find its way into the museum. The result squamous epithelium of the oesophagus are second- has been that pathologists have been describing ary to regurgitation of digestive juices, are most one thing and clinicians another, and they have commonly found in those patients where the com- had the same name. The clarification of this point petence ofthecardia has been lost through herniation has been so important, and the description of a of the stomach into the mediastinum, and have gastric ulcer in the oesophagus so confusing, that been aptly named by Barrett (1950) " reflux oeso- it would seem to be justifiable to refer to the latter phagitis." In the past there has been some dis- as Barrett's ulcer. The use of the eponym does not cussion about gastric heterotopia as a cause of imply agreement with Barrett's description of an peptic ulcer of the oesophagus, but this point was oesophagus lined with gastric mucous membrane as very largely settled when the term reflux oesophagitis " stomach." Such a usage merely replaces one was coined. It describes accurately in two words confusion by another. All would agree that the the pathology and aetiology of a condition which muscular tube extending from the pharynx down- is a common cause of digestive disorder. -
Mouth Esophagus Stomach Rectum and Anus Large Intestine Small
1 Liver The liver produces bile, which aids in digestion of fats through a dissolving process known as emulsification. In this process, bile secreted into the small intestine 4 combines with large drops of liquid fat to form Healthy tiny molecular-sized spheres. Within these spheres (micelles), pancreatic enzymes can break down fat (triglycerides) into free fatty acids. Pancreas Digestion The pancreas not only regulates blood glucose 2 levels through production of insulin, but it also manufactures enzymes necessary to break complex The digestive system consists of a long tube (alimen- 5 carbohydrates down into simple sugars (sucrases), tary canal) that varies in shape and purpose as it winds proteins into individual amino acids (proteases), and its way through the body from the mouth to the anus fats into free fatty acids (lipase). These enzymes are (see diagram). The size and shape of the digestive tract secreted into the small intestine. varies in each individual (e.g., age, size, gender, and disease state). The upper part of the GI tract includes the mouth, throat (pharynx), esophagus, and stomach. The lower Gallbladder part includes the small intestine, large intestine, The gallbladder stores bile produced in the liver appendix, and rectum. While not part of the alimentary 6 and releases it into the duodenum in varying canal, the liver, pancreas, and gallbladder are all organs concentrations. that are vital to healthy digestion. 3 Small Intestine Mouth Within the small intestine, millions of tiny finger-like When food enters the mouth, chewing breaks it 4 protrusions called villi, which are covered in hair-like down and mixes it with saliva, thus beginning the first 5 protrusions called microvilli, aid in absorption of of many steps in the digestive process. -
Tongue -Tie (Ankyloglossia) and Lip -Tie (Lip Adhesion)
Tongue -Tie (Ankyloglossia) and Lip -Tie (Lip Adhesion) What is Tongue-Tie? Most of us think of tongue -tie as a situation we find ourselves in when we are too excited to speak. Actually, tongue- tie is the non medical term for a relatively common physical condition that limits the use of the tongue, ankyloglossia. Lip -tie is a condition where the upper lip cannot be curled or moved normally. Before we are born, a strong cord of tissue that guides development of mouth structures is positioned in the center of the mouth. It is called a frenulum. As we develop, this frenulum recedes and thins. The lingual (tongue) or labial (lip) frenulum is visible and easily felt if you look in the mirror under your tongue and lip. In some children, the frenulum is especially tight or fails to recede and may cause tongue/lip mobility problems. The tongue and lip are a very complex group of muscles and are important for all oral function. For this reason having tongue tie can lead to nursing, eating, dental, or speech problems, which may be serious in some individuals. When Is Tongue and Lip- Tie a Problem That Needs Treatment? Infants A new baby with a too tight tongue and/or lip frenulum can have trouble sucking and may have poor weight gain. If they cannot make a good seal on the nipple, they may swallow air causing gas and stomach problems. Such feeding problems should be discussed with Dr. Sierra. Nursing mothers who experience significant pain while nursing or whose baby has trouble latching on should have their child evaluated for tongue and lip tie. -
Common Bile-Duct Mucosa in Choledochoduodenostomy Patients--- Histological and Histochemical Study
HPB Surgery 1988, Vol. 1, pp. 15-20 (C) 1988 Harwood Academic Publishers GmbH Reprints available directly from the publisher Printed in Great Britain Photocopying permitted by license only COMMON BILE-DUCT MUCOSA IN CHOLEDOCHODUODENOSTOMY PATIENTS--- HISTOLOGICAL AND HISTOCHEMICAL STUDY E. ELEFTHERIADIS*, V. TZIOUFA 1, K. KOTZAMPASSI and H. ALETRAS Departments of Surgery and Pathology1, University of Thessaloniki, Greece We describe the histological and histochemical changes of the common bile-duct mucosa in specimens obtained by means of peroral cholangioscopy, 1-12 years after choledochoduodenal anastomosis. Our findings- hyperplasia of the superficial epithelium, metaplastic goblet cells containing predominantly acid sialomucins, and pyloric-like gland formation containing neutral mucins- express a morphological and functional differentiation of the common bile-duct mucosa that probably facilitates its survival in a different environment. We consider that these adaptive changes may explain the uneventful long-term postoperative period of choledochoduodenostomized patients. KEY WORDS" Common bile duct, choledochoduodenal anastomosis, adaptation, peroral cholangio- scopy. INTRODUCTION After choledochoduodenal anastomosis (CDA), the common bile-duct mucosa (CBDM) is exposed to a different environment, no longer being protected by the sphincter of Oddi. Although, theoretically, this new environment i.e. gastric acid and food flowing through the anastomosis- should affect it, both clinical practice and experimental data have shown no evidence -
A Tissue-Engineered Model of the Intestinal Lacteal for Evaluating Lipid Transport by Lymphatics
ARTICLE A Tissue-Engineered Model of the Intestinal Lacteal for Evaluating Lipid Transport by Lymphatics J. Brandon Dixon,1,2 Sandeep Raghunathan,1 Melody A. Swartz1,2,3 1Institute of Bioengineering, School of Life Sciences, E´ cole Polytechnique Fe´de´rale de Lausanne (EPFL), CH-1015 Lausanne, Switzerland; telephone: þ41 21 693 9686; fax: þ41 21 693 9670; e-mail: melody.swartz@epfl.ch 2Department of Biomedical Engineering, Northwestern University, Evanston, Illinois 3Institute of Chemical Sciences and Engineering, School of Basic Sciences, EPFL, Lausanne, Switzerland Received 4 September 2008; revision received 21 February 2009; accepted 20 March 2009 Published online 1 April 2009 in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/bit.22337 trafficking, but in addition, lymphatics are central to the transport of dietary lipid from the gut. In the small intestine, ABSTRACT: Lacteals are the entry point of all dietary lipids into the circulation, yet little is known about the active enterocytes reesterify the majority of free fatty acids (FFAs) regulation of lipid uptake by these lymphatic vessels, and absorbed from the lumen of the gut into triacylglycerols there lacks in vitro models to study the lacteal—enterocyte which are then incorporated into chylomicrons (Tso and interface. We describe an in vitro model of the human Balint, 1986) and secreted basally to be picked up solely by intestinal microenvironment containing differentiated lacteals, which are blind-ended lymphatic vessels in the Caco-2 cells and lymphatic endothelial cells (LECs). We characterize the model for fatty acid, lipoprotein, albumin, center of each villus (Azzali, 1982; Schmid-Scho¨nbein, and dextran transport, and compare to qualitative uptake of 1990). -
Ost , Is Essential for Intestinal Bile Acid Transport and Homeostasis
The organic solute transporter ␣-, Ost␣-Ost, is essential for intestinal bile acid transport and homeostasis Anuradha Rao*, Jamie Haywood*, Ann L. Craddock*, Martin G. Belinsky†, Gary D. Kruh‡, and Paul A. Dawson*§ *Department of Internal Medicine, Section on Gastroenterology, Wake Forest University School of Medicine, Medical Center Boulevard, Winston–Salem, NC 27157; †Medical Science Division, Fox Chase Cancer Center, Philadelphia, PA 19111; and ‡Department of Medicine, Section of Hematology/Oncology, University of Illinois, Chicago, IL 60612 Communicated by David W. Russell, University of Texas Southwestern Medical Center, Dallas, TX, December 28, 2007 (received for review November 28, 2007) The apical sodium-dependent bile acid transporter (Asbt) is respon- Ost␣-Ost efficiently transports the major species of bile acids sible for transport across the intestinal brush border membrane; when expressed in transfected cells (3, 4); and (iv) expression of however, the carrier(s) responsible for basolateral bile acid export Ost␣ and Ost mRNA is positively regulated via the bile into the portal circulation remains to be determined. Although the acid-activated nuclear receptor farnesoid X receptor (FXR) heteromeric organic solute transporter Ost␣-Ost exhibits many (6–9), thereby providing a mechanism to ensure efficient export properties predicted for a candidate intestinal basolateral bile acid of bile acids and protection against their cytotoxic accumulation. transporter, the in vivo functions of Ost␣-Ost have not been Although these data are consistent with a role in bile acid investigated. To determine the role of Ost␣-Ost in intestinal bile transport, the in vivo functions of Ost␣-Ost have not been acid absorption, the Ost␣ gene was disrupted by homologous investigated. -
Study Guide Medical Terminology by Thea Liza Batan About the Author
Study Guide Medical Terminology By Thea Liza Batan About the Author Thea Liza Batan earned a Master of Science in Nursing Administration in 2007 from Xavier University in Cincinnati, Ohio. She has worked as a staff nurse, nurse instructor, and level department head. She currently works as a simulation coordinator and a free- lance writer specializing in nursing and healthcare. All terms mentioned in this text that are known to be trademarks or service marks have been appropriately capitalized. Use of a term in this text shouldn’t be regarded as affecting the validity of any trademark or service mark. Copyright © 2017 by Penn Foster, Inc. All rights reserved. No part of the material protected by this copyright may be reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, or by any information storage and retrieval system, without permission in writing from the copyright owner. Requests for permission to make copies of any part of the work should be mailed to Copyright Permissions, Penn Foster, 925 Oak Street, Scranton, Pennsylvania 18515. Printed in the United States of America CONTENTS INSTRUCTIONS 1 READING ASSIGNMENTS 3 LESSON 1: THE FUNDAMENTALS OF MEDICAL TERMINOLOGY 5 LESSON 2: DIAGNOSIS, INTERVENTION, AND HUMAN BODY TERMS 28 LESSON 3: MUSCULOSKELETAL, CIRCULATORY, AND RESPIRATORY SYSTEM TERMS 44 LESSON 4: DIGESTIVE, URINARY, AND REPRODUCTIVE SYSTEM TERMS 69 LESSON 5: INTEGUMENTARY, NERVOUS, AND ENDOCRINE S YSTEM TERMS 96 SELF-CHECK ANSWERS 134 © PENN FOSTER, INC. 2017 MEDICAL TERMINOLOGY PAGE III Contents INSTRUCTIONS INTRODUCTION Welcome to your course on medical terminology. You’re taking this course because you’re most likely interested in pursuing a health and science career, which entails proficiencyincommunicatingwithhealthcareprofessionalssuchasphysicians,nurses, or dentists. -
The Role of Lactic Acid in Gastric Digestion
[Reprinted from The Medical News, December 30, 1893.] THE ROLE OF LACTIC ACID IN GASTRIC DIGESTIOA ALLEN A. JONES, M.D., CLINICAL INSTRUCTOR IN MEDICINE AND INSTRUCTOR IN PRACTICE, MEDICAL DEPARTMENT, UNIVERSITY OF BUFFALO. Lactic acid is present in the stomach under nor- mal conditions from thirty to forty minutes after a test-meal composed of a roll and water or of chopped lean beef, dry bread, and water. At the expiration of that time lactic acid should entirely disappear from the stomach-contentsand free hydro- chloric acid alone should prevail. During the first thirty or forty minutes after meals the digestion of starches and albuminoids progresses quite rapidly, as may be proved by finding the middle-products and end-products of gastric digestion present, so that the presence of free lactic acid does not pro- hibit digestion. As soon as food enters the healthy stomach the secretion of hydrochloric acid is excited and it increases in amount until the production of lactic acid is checked. The exact origin of lactic acid in the healthy stomach is still a matter of debate. It may arise wholly from fermentation, or from the combination of some food-product with a secretion 1 Read before the Buffalo Academy of Medicine, November x 4) 1893. 2 from the gastric glandules, or from the gastric mucosa as a distinct secretion, although electric stimulation of the gastric glandules excites the se- cretion of hydrochloric acid and not of lactic acid. I think it arises largely from fermentation of the food, as its amount is usually proportionate to the amount of starchy, saccharine, and milk foods taken. -
Does Your Patient Have Bile Acid Malabsorption?
NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #198 NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #198 Carol Rees Parrish, MS, RDN, Series Editor Does Your Patient Have Bile Acid Malabsorption? John K. DiBaise Bile acid malabsorption is a common but underrecognized cause of chronic watery diarrhea, resulting in an incorrect diagnosis in many patients and interfering and delaying proper treatment. In this review, the synthesis, enterohepatic circulation, and function of bile acids are briefly reviewed followed by a discussion of bile acid malabsorption. Diagnostic and treatment options are also provided. INTRODUCTION n 1967, diarrhea caused by bile acids was We will first describe bile acid synthesis and first recognized and described as cholerhetic enterohepatic circulation, followed by a discussion (‘promoting bile secretion by the liver’) of disorders causing bile acid malabsorption I 1 enteropathy. Despite more than 50 years since (BAM) including their diagnosis and treatment. the initial report, bile acid diarrhea remains an underrecognized and underappreciated cause of Bile Acid Synthesis chronic diarrhea. One report found that only 6% Bile acids are produced in the liver as end products of of British gastroenterologists investigate for bile cholesterol metabolism. Bile acid synthesis occurs acid malabsorption (BAM) as part of the first-line by two pathways: the classical (neutral) pathway testing in patients with chronic diarrhea, while 61% via microsomal cholesterol 7α-hydroxylase consider the diagnosis only in selected patients (CYP7A1), or the alternative (acidic) pathway via or not at all.2 As a consequence, many patients mitochondrial sterol 27-hydroxylase (CYP27A1). are diagnosed with other causes of diarrhea or The classical pathway, which is responsible for are considered to have irritable bowel syndrome 90-95% of bile acid synthesis in humans, begins (IBS) or functional diarrhea by exclusion, thereby with 7α-hydroxylation of cholesterol catalyzed interfering with and delaying proper treatment. -
Bile Physiology
BILE PHYSIOLOGY DIPENDRA PARAJULI University of Louisville BILE COMPLEX LIPID-RICH MICELLAR SOLUTION ISO-OSMOTIC WITH PLASMA VOLUME OF HEPATIC BILE = 500 – 600 CC/DAY University of Louisville COMPOSITION University of Louisville FUNCTION OF BILE INDUCE BILE FLOW AND PHOSPHOLIPID AND CHOLESTEROL SECRETION ESSENTIAL FOR INTESTINAL ABSORPTION OF DIETARY CHOLESTEROL , FATS AND VITAMINS BIND CALCIUM AND HELP TO PREVENT Ca GALLSTONES AND OXALATE KIDNEY STONE FORMATION EXCRETION OF LIPID SOLUBLE XENOBIOTICS, DRUGS AND HEAVY UniversityMETALS of Louisville BILE FORMATION AND CIRCULATION University of Louisville University of Louisville BILE ACID SYNTHESIS TWO PATHWAYS 1) CLASSICAL / NEUTRAL - RESULTS IN THE SYNTHESIS OF APPROXIMATELY 1:1 RATIO OF CHOLIC AND CHENODEOXYCHOLIC ACIDS 2)ALTERNATE / ACIDIC - YIELDS PREDOMINANTLY UniversityCHENODEOXYCHOLIC of LouisvilleACID BILE ACID SYNTHESIS CLASSICAL / NEUTRAL PATHWAY - PREDOMINANT PATHWAY IN HEALTH - POSTCHOLECYSTECTOMY PATIENTS WITH BILE FISTULA - INFUSED WITH RADIOLABELLED PRECURSORS * [3H]7αOH CHOLESTEROL University* [3H]27-OH CHOLESTEROL of Louisville [3H]7αOH CHOLESTEROL 70-95% CONVERTED TO BILE ACIDS [3H]27-OH CHOLESTEROL <20% CONVERTED TO BIL ACIDS University of Louisville BILE ACID SYNTHESIS ALTERNATE / ACIDIC PATHWAY - MORE IMPORTANT IN CHRONIC LIVER DISEASE -CIRRHOTICS - LOW RATE OF BILE ACID SYNTHESIS - ALMOST EXCLUSIVELY UniversityCHENODEOXYCHOLIC of Louisville BILE ACID SYNTHESIS FINAL STEP = - CONJUGATION OF CHOLIC AND CHENODEOXYCHOLIC ACIDS WITH GLYCINE AND TAURINE - CONJUGATION -
Digestive Enzymes: the Key to Optimum Health
Education Article Digestive Enzymes: The Key to Optimum Health Digestion is essential for good health. Unlocking nutrients from foods is a complex process. In order to break down food we rely on optimal levels and function of a special set of proteins called digestive enzymes. These proteins are found in the saliva and also in the small intestines. Without the combined actions of our digestive enzymes we would simply be unable to absorb many nutrients that we need to maintain good health. This is why reduced levels of digestive enzymes can be linked to a wide-range of symptoms within the gut and beyond. Digestive enzymes, along with stomach acid, play a crucial role in the initial stages of digestion, i.e. the breaking down of the food that we eat. The main classes of human digestive enzymes include proteases, lipases and carbohydrases, which respectively break down the macronutrients protein, fats and carbohydrates. If we do not efficiently digest these foods then vital nutrients such as essential fats, vitamins, minerals and phytonutrients cannot be absorbed. What is more, undigested or partially digested food passes through into the large intestines and is fermented by the resident colonic bacteria, causing unpleasant symptoms such as bloating and flatulence and contributing to a toxic bowel. Naturopaths believe toxicity within the bowel is the root of all disease. We do not make digestive enzymes for every type of food that we eat, such as gluten and phytic acid found in some grains and cereals and lactose, a sugar found in milk. This means our bodies may find it difficult to digest these types of foods.