Advanced Nutrition and Dietetics in Gastroenterology E-Book

• Herausgeber: John Wiley & Sons
• Kategorie: Fachliteratur
• Serie: Advanced Nutrition and Dietetics (BDA)
• Sprache: Englisch

Seitenzahl: 929

Veröffentlichungsjahr: 2014

Beschreibung

Advanced Nutrition and Dietetics in Gastroenterology provides informative and broad-ranging coverage of the relation between nutrition and diet and the gastrointestinal tract. It explores dietary factors involved in causation of a variety of gastrointestinal disorders, as well as the effects on diet and the treatments available. It also provides an overview of anatomy and physiology, measurement and assessment of function, and dietary components relevant to gastrointestinal health.  

ABOUT THE SERIES

Dietary recommendations need to be based on solid evidence, but where can you find this information? The British Dietetic Association and the publishers of the Manual of Dietetic Practice present an essential and authoritative reference series on the evidence base relating to advanced aspects of nutrition and diet in selected clinical specialties. Each book provides a comprehensive and critical review of key literature in its subject.  Each covers established areas of understanding, current controversies and areas of future development and investigation, and is oriented around six key themes:

•Disease processes, including metabolism, physiology, and genetics
•Disease consequences, including morbidity, mortality, nutritional epidemiology and patient perspectives
•Nutritional consequences of diseases
•Nutritional assessment, drawing on anthropometric, biochemical, clinical, dietary, economic and social approaches
•Clinical investigation and management
•Nutritional and dietary management
•Trustworthy, international in scope, and accessible, Advanced Nutrition and Dietetics is a vital resource for a range of practitioners, researchers and educators in nutrition and dietetics, including dietitians, nutritionists, doctors and specialist nurses.

Leseprobe

CONTENTS

Cover

Title page

Copyright page

Series page

Preface

Foreword

Editor biographies

Contributors

SECTION 1: Physiology and function of the gastrointestinal and hepatobiliary tract

Chapter 1.1: Physiology and function of the mouth

1.1.1 Physiology

1.1.2 Measurement and assessment of function

1.1.3 Dental disease

1.1.4 Oral manifestations of gastrointestinal disease

References

Chapter 1.2: Physiology and function of the oesophagus

1.2.1 Anatomy

1.2.2 Physiology and function

1.2.3 Pathology

1.2.4 Conclusion

References

Chapter 1.3: Physiology and function of the stomach

1.3.1 Physiology, anatomy and function

1.3.2 Measurement and assessment of gastric function

1.3.3 Pathology

References

Chapter 1.4: Physiology and function of the small intestine

1.4.1 Anatomy and histology

1.4.2 Physiology and function

1.4.3 Investigation of the small intestine

1.4.4 Pathology

1.4.5 Conclusion

References

Chapter 1.5: Physiology and function of the colon

1.5.1 Anatomy

1.5.2 Function

1.5.3 Measurement and assessment of function

1.5.4 Conclusion

References

Chapter 1.6: Physiology and function of the pancreas

1.6.1 Anatomy, physiology and function

1.6.2 Measurement and assessment of function

1.6.3 Pathology

References

Chapter 1.7: Physiology and function of the hepatobiliary tract

1.7.1 Anatomy, physiology and function

1.7.2 Measurement and assessment of function

1.7.3 Pathology

References

Chapter 1.8: Gastrointestinal microbiota

1.8.1 Composition

1.8.2 Functions of the human gastrointestinal tract

1.8.3 Factors influencing composition of the microbiota

References

Chapter 1.9: Gastrointestinal tract and appetite control

1.9.1 Role of the gut neuroendocrine system in appetite regulation

1.9.2 Peptide tyrosine-tyrosine

1.9.3 Pancreatic polypeptide

1.9.4 Glucagon-like peptide 1

1.9.5 Oxyntomodulin

1.9.6 Cholecystokinin

1.9.7 Ghrelin

1.9.8 Conclusion

Acknowledgements

References

SECTION 2: Dietary components relevant to gastrointestinal health

Chapter 2.1: Fibre and gastrointestinal health

2.1.1 Classification of non-starch polysaccharides

2.1.2 Clinical effect of non-starch polysaccharides

References

Chapter 2.2: Short-chain fermentable carbohydrates

2.2.1 Gastrointestinal effects of short-chain fermentable carbohydrates

2.2.2 Short-chain fermentable carbohydrates (FODMAPs)

References

Chapter 2.3: Probiotics and the gastrointestinal microbiota

2.3.1 Criteria for classification as a probiotic

2.3.2 Safety

2.3.3 Review of different probiotics

2.3.4 Effects in the gastrointestinal tract

2.3.5 Assessing potential probiotics for efficacy

References

Chapter 2.4: Prebiotics and gastrointestinal health

2.4.1 Prebiotic definitions, characteristics and classes

2.4.2 Evidence of selective stimulation of gastrointestinal microbiota

2.4.3 Clinical applications of prebiotics

References

SECTION 3: Gastrointestinal disorders

Chapter 3.1: Orofacial granulomatosis and nutrition

3.1.1 Aetiology

3.1.2 Treatments

3.1.3 History of the cinnamon- and benzoate-free diet

3.1.4 Mechanisms involved in dietary avoidance of cinnamon and benzoates in orofacial granulomatosis

3.1.5 Sources of cinnamon and benzoates

3.1.6 Treating with a cinnamon- and benzoate-free diet

References

Chapter 3.2: Eosinophilic oesophagitis and nutrition

3.2.1 Definition

3.2.2 Typical symptoms

3.2.3 Diagnosis

3.2.4 Natural history

3.2.5 Causation – dietary or aeroallergens?

3.2.6 Dietary effects of disease

3.2.7 Treatment

3.2.8 Conclusion

References

Chapter 3.3: Gastro-oesophageal reflux disease and nutrition

3.3.1 Factors involved in causation of reflux disease

3.3.2 Dietary effects of disease or its management

3.3.3 Lifestyle and dietary treatments

References

Chapter 3.4: Oesophageal cancer and nutrition

3.4.1 Aetiology

3.4.2 Effects of disease on nutrition

3.4.3 Treatment and nutrition

3.4.4 Nutrition in the palliative setting

References

Chapter 3.5: Gastric cancer and nutrition

3.5.1 Incidence and aetiology

3.5.2 Diagnosis and staging

3.5.3 Treatment

3.5.4 Nutritional status of gastric cancer patients

3.5.5 Nutritional support

3.5.6 Nutritional status and quality of life after treatment

References

Chapter 3.6: Gastroparesis and nutrition

3.6.1 Factors involved in causation

3.6.2 Dietary effects of disease or its management

3.6.3 Investigations

3.6.4 Dietary treatments

3.6.5 Conclusion

References

Chapter 3.7: Pancreatitis and nutrition

3.7.1 Acute pancreatitis

3.7.2 Causes of pancreatitis

3.7.3 Severity of acute pancreatitis

3.7.4 Enteral nutrition

3.7.5 Parenteral nutrition

3.7.6 Postdischarge care

3.7.7 Chronic pancreatitis

Acknowledgements

References

Chapter 3.8: Pancreatic cancer and nutrition

3.8.1 Factors involved in causation

3.8.2 Dietary effects of disease and treatment

3.8.3 Dietary management

References

Chapter 3.9: Cystic fibrosis and nutrition

3.9.1 Prevalence

3.9.2 Life expectancy

3.9.3 Factors involved in causation

3.9.4 Dietary effects of the disease

3.9.5 Dietary management

3.9.6 Fibrosing colonopathy

3.9.7 Assessing efficacy of pancreatic enzyme replacement therapy

3.9.8 Distal intestinal obstruction syndrome and constipation

3.9.9 Other gastrointestinal considerations

Acknowledgement

References

Chapter 3.10: Lymphangiectasia and nutrition

3.10.1 Embryology

3.10.2 Functions of the lymphatic system

3.10.3 Aetiopathogenesis of intestinal lymphangiectasia

3.10.4 Clinical features

3.10.5 Diagnosis

3.10.6 Nutritional effects

3.10.7 Treatment

3.10.8 Conclusion

Acknowledgement

References

Chapter 3.11: Coeliac disease and nutrition

3.11.1 Diet and modernisation

3.11.2 Aetiopathogenesis and prevalence

3.11.3 Clinical features

3.11.4 Diagnosing coeliac disease

3.11.5 Dietary causes

3.11.6 Dietary and non-dietary effects

3.11.7 Dietary treatment

3.11.8 Persistent symptoms on a gluten-free diet

3.11.9 Conclusion

References

Chapter 3.12: Inflammatory bowel disease pathogenesis

3.12.1 Underlying mechanisms of immune dysregulation in inflammatory bowel disease

3.12.2 Genetic factors in the development of inflammatory bowel disease

3.12.3 Dietary risk factors in inflammatory bowel disease

3.12.4 Role of obesity in inflammatory bowel disease aetiology

3.12.5 Role of the gastrointestinal microbiota

3.12.6 Conclusion

Acknowledgement

References

Chapter 3.13: Inflammatory bowel disease nutritional consequences

3.13.1 Protein energy malnutrition

3.13.2 Body composition

3.13.3 Bone health

3.13.4 Linear growth and short stature

3.13.5 Delayed puberty

3.13.6 Micronutrient status

3.13.7 Antioxidant status

3.13.8 Anaemia

3.13.9 Aetiology of malnutrition

References

Chapter 3.14: Inflammatory bowel disease dietary management

3.14.1 Dietary management of Crohn’s disease

3.14.2 Dietary management of ulcerative colitis

3.14.3 Conclusion: role of dietary treatment in inflammatory bowel disease

References

Chapter 3.15: Lactose malabsorption and nutrition

3.15.1 Lactase persistence

3.15.2 Implications for diet today

3.15.3 Conclusion

References

Chapter 3.16: Intestinal failure and nutrition

3.16.1 Consequences of intestinal failure and short bowel

3.16.2 Fluid and electrolyte management in short bowel

3.16.3 Pharmaceutical management

3.16.4 Adaptation

3.16.5 Nutritional management

3.16.6 Dietary management of jejunocolic anastomosis

3.16.7 Dietary management of patients with a jejunostomy

3.16.8 Oral nutritional supplements and enteral nutrition

3.16.9 Micronutrient deficiencies

3.16.10 Dietary management of enterocutaneous fistula

3.16.11 Intestinal transplantation and tissue engineering

References

Chapter 3.17: Stomas and nutrition

3.17.1 Preoperative nutritional status

3.17.2 Perioperative nutrition and enhanced recovery after surgery

3.17.3 Colostomy

3.17.4 Ileostomy

References

Websites

Chapter 3.18: Irritable bowel syndrome pathogenesis

3.18.1 Genetic factors

3.18.2 Psychological factors

3.18.3 Visceral hypersensitivity

3.18.4 Inflammatory mechanisms and dietary components

3.18.5 Food hypersensitivity

3.18.6 Gastrointestinal microbiota

3.18.7 Conclusion

References

Chapter 3.19: Irritable bowel syndrome dietary management

3.19.1 Dietary effects of disease or its management

3.19.2 Dietary interventions

3.19.3 Food allergy

3.19.4 Pharmacological food intolerance

3.19.5 Other exclusion diets

3.19.6 Probiotics

3.19.7 Prebiotics

3.19.8 Conclusion

References

Chapter 3.20: Diverticular disease and nutrition

3.20.1 Dietary factors involved in causation

3.20.2 Dietary effects of disease or its management

3.20.3 Dietary management

References

Chapter 3.21: Constipation and nutrition

3.21.1 Definitions and types

3.21.2 Factors involved in causation

3.21.3 Dietary effects of disease or its management

3.21.4 Dietary treatments

References

Chapter 3.22: Colorectal cancer and nutrition

3.22.1 Factors involved in causation

3.22.2 Nutritional status of colorectal cancer patients

3.22.3 Medical treatment of colorectal cancer

References

SECTION 4: Hepatobiliary disorders

Chapter 4.1: Gallbladder disease and nutrition

4.1.1 Gallstones

4.1.2 Factors involved in causation

4.1.3 Nutritional management

4.1.4 Functional dyskinesia of the gallbladder

4.1.5 Steatocholecystitis

4.1.6 Gallbladder cancer

References

Chapter 4.2: Primary biliary cirrhosis and primary sclerosing cholangitis and nutrition

4.2.1 Factors involved in causation

4.2.2 Nutritional consequences

4.2.3 Dietary management

References

Chapter 4.3: Alcohol-related liver disease and nutrition

4.3.1 Alcoholic hepatitis

4.3.2 Alcoholic liver disease

4.3.3 Steatosis – fatty liver

4.3.4 Fibrosis

4.3.5 Alcoholic cirrhosis

References

Chapter 4.4: Autoimmune hepatitis and viral hepatitis and nutrition

4.4.1 Autoimmune hepatitis

4.4.2 Viral hepatitis

References

Chapter 4.5: Non-alcoholic fatty liver disease and hereditary haemochromatosis and nutrition

4.5.1 Non-alcoholic fatty liver disease

4.5.2 Hereditary haemochromatosis

References

Chapter 4.6: Decompensated liver disease and nutrition

4.6.1 Dietary causes and effects of decompensated liver disease

4.6.2 Dietary causes of hepatic encephalopathy

4.6.3 Nutritional consequences of ascites

4.6.4 Dietary management of decompensated liver disease

4.6.5 Dietary management of hepatic encephalopathy

4.6.6 Dietary management of ascites

References

Chapter 4.7: Hepatocellular carcinoma and nutrition

4.7.1 Treatments

4.7.2 Nutritional consequences of palliative treatments

4.7.3 Nutritional requirements

References

Chapter 4.8: Liver transplantation and nutrition

4.8.1 Nutritional status pre-transplant

4.8.2 Nutritional requirements and feeding immediately post transplant

4.8.3 Metabolic syndrome post liver transplant

4.8.4 Bone disease

4.8.5 Probiotics

4.8.6 Drug–nutrient interactions

4.8.7 Recurrence of diseases

4.8.8 Food safety post transplantation

References

Index

End User License Agreement

List of Tables

Chapter 1.1

Table 1.1.1 Contribution of groups of salivary glands to overall saliva production at rest and during eating

Chapter 1.4

Table 1.4.1 Differences in the ultrastructure and function of the small intestine

Table 1.4.2 Causes of malabsorption

Table 1.4.3 Clinical consequences of specific micronutrient deficiencies

Chapter 1.8

Table 1.8.1 Summary of microbiota associated with the GI tract in humans

Chapter 2.1

Table 2.1.1 Classification of non-starch polysaccharides based on three physicochemical characteristics [5,8,55]

Table 2.1.2 Potential effects of fibre on components of the gastrointestinal barrier and on bacterial translocation, and possible mechanisms

Chapter 2.2

Table 2.2.1 Classification of dietary carbohydrates

Table 2.2.2 Dietary carbohydrates classified according to digestibility

Table 2.2.3 Details of FODMAPs

Table 2.2.4 Examples of high FODMAP foods

Table 2.2.5 Examples of low FODMAP foods (

a

indicates foods that contain a lesser amount of FODMAPs – these can be eaten, but not in large amounts)

Chapter 2.4

Table 2.4.1 Selection of compounds with proven prebiotic properties

Table 2.4.2 Clinical trials of prebiotic supplementation in a range of gastrointestinal disorders

Chapter 3.1

Table 3.1.1 Preservatives to be avoided on the cinnamon- and benzoate-free diet

Table 3.1.2 Main sources of cinnamon and benzoates

Chapter 3.5

Table 3.5.1 European Society of Parenteral and Enteral Nutrition guidelines on enteral nutrition – non-surgical oncology [27]

Chapter 3.9

Table 3.9.1 Recommended starting doses of fat-soluble vitamins in pancreatic insufficient patients with cystic fibrosis

Chapter 3.13

Table 3.13.1 Major circulating concentrations of multiple micronutrients in patients with inflammatory bowel disease

Chapter 3.14

Table 3.14.1 Overview of guidelines for the provision of enteral nutrition as primary therapy in Crohn’s disease

Table 3.14.2 The LOFFLEX exclusion diet: summary of foods allowed and not allowed

Table 3.14.3 Summary of the dietary management of Crohn’s disease (CD) and ulcerative colitis (UC)

Chapter 3.15

Table 3.15.1 Lactose content in different type of products (adapted from Holland et al. [53], with permission from the Royal Society of Chemistry)

Chapter 3.16

Table 3.16.1 Recommendations for the dietary treatment of patients with short bowel

Chapter 3.17

Table 3.17.1 Conditions which may require stoma formation

Table 3.17.2 Dietary effects on stoma output

Table 3.17.3 Dietary recommendations for colostomy and ileostomy

Chapter 3.20

Table 3.20.1 Definition of terms in diverticular disease

Chapter 3.21

Table 3.21.1 Probiotic strains and their beneficial effects on constipation

Chapter 4.1

Table 4.1.1 Worldwide prevalence

a

of gallstones

Table 4.1.2 Non-nutritional factors influencing the formation of gallstones

Chapter 4.2

Table 4.2.1 Recommendations from EASL and AASLD for bone density scanning, calcium and fat-soluble vitamin supplementation for those with PBC and PSC

Table 4.2.2 Measurement and sources of fat-soluble vitamins

Chapter 4.5

Table 4.5.1 Waist circumference levels for central obesity

Table 4.5.2 Causes of non-alcoholic fatty liver disease

Table 4.5.3 Potential beneficial effect of diet-induced weight loss on non-alcoholic fatty liver disease

Chapter 4.6

Table 4.6.1 Types of liver disease

Table 4.6.2 An estimate of the weight of ascites and peripheral oedema [26]

Table 4.6.3 Energy and protein requirements for people with liver disease

Chapter 4.8

Table 4.8.1 Indications for liver transplantation

List of Illustrations

Chapter 1.2

Figure 1.2.1 High-resolution manometry of a normal swallow, with pressure data presented as a spatiotemporal plot. Sensors are spaced at <2 cm intervals which provide a vivid depiction of oesophageal pressure activity from the pharynx to the stomach with changes in pressure represented as changes in colour (in clinical practice). Deglutitive inhibition is seen as the synchronous relaxation of the upper oesophageal sphincter (UOS) and lower oesophageal sphincter (LOS) followed by a co-ordinated peristalsis with increasing pressure duration as it progresses distally. Important landmarks are highlighted. Images acquired by 36-channel SSI Manoscan 360. IBP, intrabolus pressure.

Figure 1.2.2 Transient lower oesophageal sphincter relaxation followed shortly afterwards by a common cavity during which there is equalisation of pressure between the stomach and oesophagus when reflux is most likely to occur. The event is terminated and the oesophagus is cleared of refluxed contents with the arrival of a well-co-ordinated primary peristalsis. Oesophageal and lower oesophageal sphincter pressures return to baseline levels following completion of peristalsis. TLOSR, transient lower oesophageal sphincter relaxation.

Figure 1.2.3 Bravo delivery system. The delivery device (A, B) is normally inserted orally through the pharynx. Markings on the delivery device depict the distance from the incisors. The capsule is deployed at the proximal LOS high-pressure zone (C). The receiver remains with the patient (via belt clip or shoulder pouch) for the duration of the study (D). The capsule falls off spontaneously at a median of 5 days. Complications requiring its early removal are rare.

Chapter 1.3

Figure 1.3.1 Schematic diagram of the human stomach.

Chapter 1.4

Figure 1.4.1 Structure of the small intestine.

Chapter 1.9

Figure 1.9.1 Mechanism of gut hormone action. Hormones released from the gastrointestinal tract into the circulation act on the brain to modulate appetite. Three sites are known to be of key importance: the hypothalamus, brainstem and vagus nerve. AgRP, agouti-related peptide; CART, cocaine- and amphetamine-regulated transcript; CCK, cholecystokinin; GLP-1, glucagon-like peptide 1; NPY, neuropeptide Y; POMC, pro-opiomelanocortin; OXM, oxyntomodulin; PP, pancreatic polypeptide; PYY, peptide tyrosine-tyrosine.

Chapter 2.1

Figure 2.1.1 Modulation of mucus barrier dynamics by luminal factors in the intestine. A complex interplay of luminal factors of bacterial, endogenous and dietary origin results in luminal bulk and mucus degradation. The epithelium may respond to increased or decreased luminal stress by altering rates of mucin granule exocytosis, mucin mRNA synthesis or goblet cell proliferation. Luminal stress triggers three putative pathways that result in an epithelial response. 1. Shear stress or colonic distension results in triggering of the mucosal mechanoreceptors. 2. Prostaglandins or acetylcholine are released as a result of either increased luminal bulk or enteroendocrine cell response to changes in the luminal milieu. 3. Direct (e.g. bacterial adherence to epithelium) or indirect (e.g. chains to bacterial by-products) sensing of changes to the luminal bacterial populations by the GALT results in an immune-type response, driven by interleukins or other local mediators. These three pathways appear to drive different epithelial responses that drive mucin secretion. Within mucin production, proteins are synthesised with the rough endoplasmic reticulum, then glycosylated and polymerised. Prior to encapsulation in secretory vesicles, mucins are tightly packed into granules, in high calcium ion (

black dots

) concentration. As the vesicles join to the apical membrane, mucins rapidly swell upon hydration and separate from Ca

++

. ER, endoplasmic reticulum; LPS, lipopolysaccharide; PGE, prostaglandins; SCFA, short-chain fatty acids.

Figure 2.1.2 Roles of fibre in colon cancer protection. Source: Niba & Niba [54]. Reproduced with permission from Emerald Group Publishing Ltd. NDOs Non-digestible oligosaccharides.

Chapter 3.5

Figure 3.5.1 Stomach cancer: world age-standardised incidence and mortality rates, males, regions of the world, 2008 estimates [1]. Reproduced with permission from Cancer Research UK.

Figure 3.5.2 Stomach cancer: world age-standardised incidence and mortality rates, females, regions of the world, 2008 estimates. Reproduced with permission from Cancer Research UK.

Chapter 3.10

Figure 3.10.1 Patient profile before starting treatment. Reproduced with permission from Dr Babu Vadamalayan, King's College Hospital, London.

Figure 3.10.2 Enteroscopy picture showing lymphangiectasia-like changes. Reproduced with permission from Dr Babu Vadamalayan, King's College Hospital, London.

Chapter 3.11

Figure 3.11.1 The coeliac iceberg, model showing the hidden forms of coeliac disease that lie below the waterline. HLA, human leucocyte antigen.

Figure 3.11.2 Investigation of the patient with non-responsive coeliac disease Diagnostic algorithm for non-responsive coeliac disease. FHx, family history; FODMAPs, fermentable oligosaccharides, disaccharides, monosaccharides and polyols; HLA, human leucocyte antigen; SIBO, small intestinal bacterial overgrowth; PLE, protein-losing enteropathy; RCD.

Chapter 3.12

Figure 3.12.1 Interaction of various factors that are known to lead to chronic intestinal inflammation.

Figure 3.12.2 The link of inflammatory signalling response in various tissues to the development of obesity-related alterations, neurodegenerative disease and autoimmunity that are all influenced by host genetics, diet composition, immune system and microbiota. Modified from Renz et al. [78].

Figure 3.12.3 Possible genetic and non-genetic factors that are involved in Crohn’s disease pathogenesis. BMI, Body Mass Index; CNV, copy number variant; SNP, single nucleotide polymorphism.

Chapter 3.13

Figure 3.13.1 The aetiology and presentation of malnutrition in IBD. GI, gastrointestinal; IBD, inflammatory bowel disease.

Chapter 3.14

Figure 3.14.1 Causes of undernutrition in IBD, inflammatory bowel disease. Adapted from O'Sullivan [26].

Chapter 3.15

Figure 3.15.1 Interpolated map of LP phenotype distribution in the ‘Old World’. Data points (dots) were taken from the literature (for details see Ingram et al. [6]). The key shows the frequency of the LP phenotype, black being used for the lowest frequency while white is used for the highest. Source: Itan et al. [7]. Reproduced with permission from BioMed Central Ltd.

Chapter 3.19

Figure 3.19.1 Algorithm for dietary management of IBS. BMI, Body Mass Index; CHO, carbohydrate; IBS-C, constipation-dominant irritable bowel syndrome.

Chapter 3.20

Figure 3.20.1 Pathogenetic events leading from diverticulosis to diverticular disease. Source: Tursi and Papagrigoriadis [4].

Chapter 4.5

Figure 4.5.1 Stages of non-alcoholic fatty liver disease.

Figure 4.5.2 Two-hit theory of obesity-related hepatic fibrosis. FFA, free fatty acids; TG, triglyceride; TNF, tumour necrosis factor.

Chapter 4.6

Figure 4.6.1 The major metabolic changes that occur in someone with cirrhosis [7–13].

Guide

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Advanced Nutrition and Dietetics in Gastroenterology

Editor

Miranda Lomer PhD RD

Series Editor

Kevin Whelan PhD RD

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Library of Congress Cataloging-in-Publication Data

Advanced nutrition and dietetics in gastroenterology / editor, Miranda Lomer.  1 online resource. Includes bibliographical references and index. Description based on print version record and CIP data provided by publisher; resource not viewed. ISBN 978-1-118-87289-5 (ePub) – ISBN 978-1-118-87291-8 (Adobe PDF) – ISBN 978-0-470-67132-0 I. Lomer, Miranda, editor. [DNLM: 1. Digestive System Diseases. 2. Dietetics. 3. Digestive System Physiological Phenomena. 4. Nutrition Therapy. 5. Nutritional Status. WI 140] RC801 616.3′3–dc23

2014006436

A catalogue record for this book is available from the British Library.

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Advanced Nutrition and Dietetics BOOK Series

Dietary recommendations need to be based on solid evidence, but where can you find this information? The British Dietetic Association and the publishers of the Manual of Dietetic Practice present an essential and authoritative reference series on the evidence base relating to advanced aspects of nutrition and dietetics in selected clinical specialties. Each book provides a comprehensive and critical review of key literature in the area. Each covers established areas of understanding, current controversies and areas of future development and investigation, and is oriented around six key themes:

Disease processes, including metabolism, physiology and genetics

Disease consequences, including morbidity, mortality and patient perspectives

Clinical investigation and management

Nutritional consequences of disease

Nutritional assessment, including anthropometric, biochemical, clinical, dietary, economic and social approaches

Nutritional and dietary management of disease

Preface

In recent years there has been an overwhelming interest in the role of diet and nutrition in gastrointestinal health and disease. There are a number of general books that focus on combining these topics but not specifically at an advanced level. The aim of this book is to be an essential and authoritative reference and review for an international audience of health professionals involved in the management or research of patients with gastrointestinal disorders.