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Nutrition in the Prevention and Treatment of Abdominal Obesity
Summary
Nutrition in the Prevention and Treatment of Abdominal Obesity focuses on the important roles that exercise, dietary changes, and foods play in promoting as well as reducing visceral fat. Nutritionists, dieticians, and healthcare providers seeking to address the abdominal obesity epidemic will use this comprehensive resource as a tool in their long-term goal of preventing chronic diseases, especially heart, vascular, and diabetic diseases.
Experts from a broad range of disciplines are involved in dealing with the consequences of excessive abdominal fat: cardiology, diabetes research, studies of lipids, endocrinology and metabolism, nutrition, obesity, and exercise physiology. They have contributed chapters that define a range of dietary approaches to reducing risk and associated chronic diseases. They begin by defining visceral obesity and its major outcomes; they also discuss the importance and the challenges of dietary approaches to reduce abdominal obesity, as compared to clinical approaches, with major costs and risks.
Offers detailed, well-documented reviews outlining the various dietary approaches to visceral obesity with their benefits and failures Includes chapters on types of foods, exercise, and supplements in reducing obesity and its chronic clinical companions, especially diabetes and cardiovascular disease Helps nutritionists, dieticians, and healthcare providers approach patients in making decision about nutritional therapies and clinical treatments for abdominal obesity, from an evidence-based perspectiveRead on the Scribd mobile app
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Nutrition in the Prevention and Treatment of Abdominal Obesity
Nutrition in the Prevention and Treatment of Abdominal Obesity
First Edition
Ronald Ross Watson
University of Arizona, Division of Health Promotion Sciences, Mel and Enid Zuckerman College of Public Health, and School of Medicine, Arizona Health Sciences Center, Tucson, AZ, USA
Table of Contents
Cover image
Title page
Copyright
Preface
Acknowledgments
Contributors
1: Epidemiology and Clinical Management of Visceral Obesity
A: Epidemiology and Pathophysiology of Abdominal Obesity
1: Diet and Irritable Bowel Syndrome, with a Focus on Appetite-Regulating Gut Hormones
Introduction
Diet Intake in Irritable Bowel Syndrome Patients
The Role of Diet in the Development of IBS Symptoms
Abnormalities in the Endocrine System of the Gut in Irritable Bowel Syndrome
Irritable Bowel Syndrome and Appetite-Regulating Gut Hormones
Effect of Dietary Guidance
Conclusion
2: Work and Abdominal Obesity Risk
Occupational Status
Job Strain
Occupational Physical Activity
Shift Work
Unemployment
Conclusion
3: Effects of Dietary Patterns and Physical Activity on the Establishment of Abdominal Obesity in Adolescents
Abdominal Obesity in Adolescents
Meal Patterns, Foods, and Abdominal Obesity in Adolescents
Physical Activity and Abdominal Obesity in Adolescents
Conclusions
4: Lifestyle Factors Affecting Abdominal Obesity in Children and Adolescents: Risks and Benefits
Introduction
Physical Activity and Abdominal Obesity
Sedentary Activities
Sleep Duration
Nutrition
Alcohol Consumption
Smoking
Conclusion
5: Female Cancer Survivorship and Obesity
Obesity and Female Cancer
Female Cancer Survivorship
Physical Activity
Diet Considerations
Future Directions
6: Evaluation of Visceral Fat in Massive Obesity
Anthropometric Assessments
Physical Methods to Assess Massive Abdominal Obesity
Biological Parameters
Histological Markers in Adipose Tissue
Other Methods Used to Assess Abdominal Fat Repartition
Conclusion
7: Beyond Nutrition Is There Any Role for Physical Activity in Nonalcoholic Fatty Liver Disease Therapy?
Introduction
The Measurement of Subcutaneous and Visceral Adipose Tissue
Physical Activity
The Influence of Physical Activity on Subcutaneous and Visceral Adipose Tissue
Age and Gender Differences in the Response of Subcutaneous and Visceral Adipose Tissue to Physical Activity
Physiological Effect of Exercise on Obesity and Subcutaneous and Visceral Adipose Tissue
Nonalcoholic Fatty Liver Disease, Physical Activity, and Adipose Tissue
Concluding Remarks
8: Abdominal Fat and African-Americans: Incidence and Relationship to Disease
Introduction
Incidence of Abdominal Obesity and Cardiometabolic Risk: African-American Adults
Incidence of Abdominal Obesity and Cardiometabolic Risk: African-American Children and Adolescents
Intervention Strategies
Conclusions
B: Abdominal Obesity and Metabolic Syndrome
9: Visceral Fat and Hypertension: Sex Differences
Overview
Sex Differences in Quantity and Distribution of Visceral and Subcutaneous Fat
Sex Differences in Cellularity and Secretory Profiles of Visceral and Subcutaneous Fat
Sex Differences in Obesity-Induced Hypertension
Conclusion
10: Remission of Metabolic Syndrome After Sleeve Gastrectomy
Effect of Laparoscopic Sleeve Gastrectomy on Type 2 Diabetes Mellitus
Effect of Laparoscopic Sleeve Gastrectomy on Lipid Profile
Effect of Laparoscopic Sleeve Gastrectomy on Hypertension
Effect of Laparoscopic Sleeve Gastrectomy on Cortisol Levels
11: Serum Magnesium and Abdominal Obesity and its Consequences
Introduction
Magnesium Deficiency and its Health-Associated Consequences
Abdominal Obesity
Mechanism of Magnesium Deficiency in Obesity
Magnesium and Abdominal Obesity
Conclusion
C: Nutrition, abdominal obesity, and type 2 diabetes
12: Abdominal Adipose Tissue and Insulin Resistance: The Role of Ethnicity
Introduction
Abdominal Adipose Tissue
Defining Ethnicity
Ethnicity and Insulin Resistance
Ethnicity and Abdominal Adiposity
Ethnic Differences in the Association Between Abdominal Adipose Tissue and Insulin Resistance
Conclusions
13: Visceral Fat Predicts Ectopic Fat Accumulation Mechanisms and Health Consequences
Introduction
Predictors of Ectopic Fat Deposition
Weight Loss, Visceral Fat, and Ectopic Fat Deposition
Health Consequences of Visceral Adipose Tissue and Ectopic Fat Deposition
14: Blood Pressure Regulation in Abdominal Obesity
Introduction
Obesity: A Definition
Systemic Hypertension: A Definition
Which Adiposity Index is the Best for Explaining the Link between Systemic Hypertension Risk and Obesity?
Abdominal Obesity and its Impact on Blood Pressure
Hemodynamic Pattern: Mechanisms
Abdominal Obesity and Exercised-Induced Hypertension
Adipokines
Metabolic Syndrome: a Combination of Cardiovascular Risk Factors Including High Blood Pressure
Management of Systemic Hypertension in Obesity: Benefits from Weight Reduction
A Discovery Emerging from Aggressive Diet and Exercise Therapy in Abdominal Obesity
Conclusion
2: Diet, Supplements, and Foods in the Management of Visceral Obesity
D: Mechanisms of Altering Abdominal Obesity
15: Effect of Glucagon-Like Peptide 1 Receptor Agonists on Visceral Fat Adiposity, Appetite, and Food Preference
Introduction
Central and Peripheral Actions of GLP-1 on Appetite and Food Intake
Effects on Body Weight
Effects on Body Fat Composition
Effects on Food Preference and Eating Behavior
Conclusions
16: Effects of Sleeve Gastrectomy on Calcium Metabolism
Changes in Nutritional Status
Effects on Calcium Levels
Effects on Vitamin D Levels
Effects on Parathyroid Hormone Levels
Effects on Bone Mineral Density
17: Intermittent Versus Daily Calorie Restriction in Visceral Fat Loss
Introduction
Methods
Results
Discussion
Conflicts of Interest
18: Stress-Induced Eating Dampens Physiological and Behavioral Stress Responses
Introduction
Glucocorticoids and Insulin Promote Stress-Induced Eating
Glucocorticoids and Insulin Promote Visceral Fat Accumulation
Stress-Induced Eating Dampens Physiological and Behavioral Stress Responses
Reinforcement of Stress-Induced Eating via Affective Responses, the Reward System, and Enhanced Memory
Role of Glucocorticoids and Visceral Fat in Dampening Stress Responses
Conclusion and Future Directions
19: Fructose-Induced Hypertriglyceridemia: A Review
Introduction
Therapeutics
Summary
20: Impact of Sex and Lifestyle of Adolescents and Their Parents on Obesity
Introduction
Methods
Results
Discussion
Conclusion
21: Physical Activity, Inflammatory Cytokines, Endothelial Dysfunction, and Risk of Coronary Artery Diseases in Visceral Obesity
Introduction
Disturbances to Endothelial Function and Cardiovascular Inflammatory Pathways in Visceral Obesity
Physical Activity Preserves Endothelial Dysfunction and Exerts Anti-Inflammatory Effects
Conclusion
E: Dietary Foods and Visceral Fat Accumulation and Removal
22: Fermented Soypastes, Doenjang and Cheonggukjang, and Obesity
Soybean and Fermented Soypaste
Antiobesity Effects of Isoflavones
Mechanisms Involved in Fermented Soypaste Antiobesity Activity
Antiobesity Effects of Fermented Soypastes in Rodents
Antiobesity Effects of Fermented Soypastes in Humans
Conclusion and Future Research Perspectives
23: Alcohol Intake and Hormonal Dysregulation of Food Intake in Visceral Fat Accumulation
Background
Alcohol Metabolism
Alcohol Intake and Appetite Control
Alcohol Consumption and Hormonal Deregulation
Effects of Alcohol Consumption and Abstinence on Appetite Regulation
Conclusions
24: Coffee Intake and Obesity
Obesity, Coffee Consumption, and Active Compounds
Coffee and Reduction of Obesity Risk: A Vision from Epidemiological Studies
Coffee and its Components
Coffee and the Mechanisms that Underlie its Protective Effects Against Obesity
Potential Adverse Effects of Coffee
Conclusion
25: Bread Intake and Abdominal Fat
Introduction
Scientific Evidence
Cross-Sectional Studies
Longitudinal Studies
Intervention Studies
Summary of The Scientific Evidence about the Influence of Bread Consumption on Abdominal Obesity
Influence of Bread Consumption on Abdominal Obesity Prevention
Influence of Bread Consumption on Abdominal Obesity Treatment
Effects of Low-Carbohydrate vs. Low-Fat Diets
Hypotheses on the Mechanism of Action by Which Bread Consumption Influences Abdominal Obesity
Energy Density
Glycemic Index
Dietary Fiber
Gut Microbiota
Conclusions
26: Role of the Immune System in Obesity-Associated Inflammation and Insulin Resistance
Introduction
Inflammatory Changes in Obesity and Insulin Resistance
Inflammatory Changes of Adipocytes and Immune Cells in the Adipose Tissue Microenvironment
Signaling Molecules that Induce or Reduce Obesity-Associated Inflammation and Insulin Resistance
GPR120
Immunotherapy for Insulin Resistance
Concluding Remarks
27: Metabolic Effects of Abdominal Fats in Animal Models and Humans
Obesity
Adipose Tissue: Body Fat
Body Size, Function, and Health
Abdominal Obesity and Cardiovascular Diseases
Adipose Tissue and Inflammation
Intra-Abdominal Obesity and Diabetes
Abdominal Obesity and Cancer
Abdominal Obesity and Aging
Summary
28: Appetite and Reward Signals in the Brain: Sugar Intake Effects on Brain Activity as Measured by Functional Magnetic Resonance Imaging
Introduction
Taste and Reward
Conclusions
F: Dietary Supplements and Visceral Obesity
29: Flaxseed Secoisolariciresinol Diglucoside and Visceral Obesity
30: Carotenoids as a Nutraceutical Therapy for Visceral Obesity
Introduction
Carotenoids
Antiobesity Effect of Fucoxanthin
Accumulation of Fucoxanthin Metabolites in Abdominal White Adipose Tissue
UCP 1 Induction in Abdominal White Adipose Tissue by Fucoxanthin
Downregulation of Insulin Resistance-Inducing Adipocytokines in Abdominal White Adipose Tissue by Fucoxanthin
Fucoxanthin Upregulates GLUT4 in Skeletal Muscle
Fucoxanthin Intake Improves Glucose Level and Has in Vivo Antioxidant Activity
Conclusion
31: Nutritional Deficiencies in Obese Sleeve Gastrectomy Patients
Introduction
Sleeve Gastrectomy: Dietary Restriction and Associated Mechanisms
Preoperative Nutritional Deficiencies in Bariatric Surgery Candidates
Postoperative Nutritional Deficiencies After Sleeve Gastrectomy
Micronutrient Supplementation
Recommendations for Nutrition Care After Sleeve Gastrectomy
G: Macromolecules in Foods and Diets and Abdominal Obesity
32: Dairy Whey Proteins and Obesity
Introduction
Whey Proteins and Health
Metabolic Effects of Whey Proteins
Conclusion
33: Probiotics to Treat Visceral Obesity and Related Liver Disease
Introduction
Metabolic Syndrome
Obesity Pathogenesis
Intestinal Microbiota and the Gut-Liver Axis
Microbiota, Gut-Liver Axis, and Nonalcoholic Fatty Liver Disease
Fructose, Obesity, and Liver Involvement
Intestinal MicRObiota and Gut-Liver Axis Manipulation by Probiotics
Probiotics, Obesity, and Visceral Fat Disorders
Probiotics Use in Fatty Liver Disease
Conclusions
34: Beta-Cryptoxanthin, a Novel Carotenoid Derived from Satsuma Mandarin, Prevents Abdominal Obesity
Introduction
Epidemiology of beta-cryptoxanthin
Industrial production of beta-cryptoxanthin
Beta-cryptoxanthin and obesity
Beta-cryptoxanthin reduces the visceral fat in mildly obese humans
The mechanism of beta-cryptoxanthin-dependent obesity prevention
Conclusion
35: A Diet with Carbohydrates Eaten Primarily at Dinner: an Innovative, Nutritional Approach to End the Vicious Cycle of Abdominal Obesity
The Vicious Cycle of Abdominal Obesity and the Metabolic Syndrome
Fat Tissue as an Endocrine Organ and Its Influence on Food Intake and the Metabolic Syndrome
Studies in Muslim Populations during Ramadan
The Effect of a Diet with Carbohydrates Eaten Primarily at Dinner on Abdominal Obesity, Insulin Resistance, and the Metabolic Syndrome: Basic Research
Future Research: Understanding the Physiological Mechanisms
Dietary Alternatives to Replace Medications: Nutrition Targeting
Interim Conclusions
H: Micromolecules and Nutrients as Modulators of Visceral Fat
36: Effects of Different Dietary Fatty Acids on Human Energy Balance, Body Weight, Fat Mass, and Abdominal Fat
Introduction
Dietary Fat and Human Energy Balance
Physiological Effects of Different Dietary Fat Subtypes
Conclusions and Recommendations
37: Conjugated Linoleic Acid in Human Health Effects on Weight Control
Introduction
Discovery and Origins of Conjugated Linoleic Acid
Antiobesity Effects of Conjugated Linoleic Acid
Other Health Benefits of Conjugated Linoleic Acid
Conclusion
38: Essential Amino Acid Supplementation for the Prevention and Treatment of Obesity
Macronutrients and Obesity
Essential Amino Acids and the Control of Satiety
Amino Acids and the Preservation or Augmentation of Lean Body Mass in Obese Individuals
Conclusions
Conflict of interest statement
I: Activity of Adipocytes: Role in Growth and Accumulation of Fat
39: Fibroblast Growth Factor 21 is a Regulator of Energy Metabolism in the Liver and Adipose Tissue
Background
FGF-21 Structure, Expression, and Receptor Binding
Paracrine/Autocrine, Endocrine, and Pharmacological Roles of FGF-21
Expression and Regulation of FGF-21
Physiological Role of FGF-21
The Role of FGF-21 in Human Metabolic Diseases
FGF-21-Targeted Therapy
Conflict of interest statement
40: Genetics of Abdominal Obesity
Introduction
Heritability
Monogenic Obesity
Genome-wide Linkage Study
Candidate Gene Association Study
Genome-wide Association Study
Gene-environment Interactions
Sexual Dimorphism
Epigenetics
Conclusions
41: The Role of Site-Specific Adipose Tissue Fatty Acid Composition in Obesity
Fatty Acid Composition of Adipose Tissue
Which Factors Determine Adipose Tissue Fatty Acid Profile?
Adipose Tissue Fatty Acids and Obesity
Adipose Tissue Fatty Acid Composition as a Predictor of Weight Loss
Summary
J: Fiber and Visceral Obesity
42: Using Psyllium to Prevent and Treat Obesity Comorbidities
Introduction
Psyllium and Health
Body Composition and Appetite
Blood Sugar Levels and Insulin Regulation
Blood Lipids
Vascular Function
Conclusion
Conflict of Interest Statement
43: Whole Grains in the Prevention and Treatment of Abdominal Obesity
Introduction
Biological Plausibility of Whole Grain-Mediated Effects on Adiposity
Associations between Whole-Grain Intake and Adiposity in Observational Studies
Evidence from Clinical Trials of Whole Grain-Mediated Effects on Adiposity
Conclusion
Index
Copyright
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Preface
Abdominal or visceral fat comprises fat deposits between the liver and kidneys that are packed into the abdominal cavity. This fat is distinct from subcutaneous and intramuscular fat because it is primarily visceral and includes several adipose depots. Historically, such fat has a played a key role in survival in times of famine. As described in the book, such fat is subject to lifestyle management as well as to accumulation.
Epidemiology and Clinical Management of Abdominal Obesity
Appetite-regulating gut hormones, work, diet, and physical activity in adults, children, and adolescents have all been described as factors that affect abdominal fat accumulation. Tarantino describes the efficacy of physical activity in treating nonalcoholic fatty liver disease. Its actions in specific populations, for example the elevated hypertension of African-Americans, are defined and explained by Hornbuckle. Von Gruenigen shows how fat plays a role in cancer survivorship, while Clement reviews massive obesity and its consequences. Clearly, and historically, lifestyle factors are major factors that affect abdominal fat; these are defined by Suliga with Gomez-Martinez in their review of the role of physical activity in abdominal obesity in adolescents. Therapies including surgery and sleeve gastrostomy are reviewed by Ruiz-Tovar, while the beneficial effects of supplemental magnesium are defined by Kokot.
Fat is constantly being stored and released from adipose tissue. Storage in adipose tissue is regulated by insulin and stimulated by high serum glucose. Thus, fat cells have an important role in maintaining triglyceride and free fatty acid levels. However, abdominal fat is more prone to inducing insulin resistance; therefore, central obesity is a marker of impaired glucose tolerance as a risk factor for many obesity-related diseases. Gasevic et al. show that adipose tissue affects insulin resistance and is further modified by ethnicity. In addition, Rossi and colleagues describe visceral fat as key to ectopic fat accumulation, while Leblanc and Poirier discuss how high blood pressure risk is lessened by reducing visceral obesity. Finally, Prasad defines the problems of advanced glycation end-products in relation to adiposity.
Diet, Supplements, and Foods in the Management of Visceral Obesity
Understanding abdominal obesity will promote its modification and prevention, thus reducing chronic disease levels. Under standard conditions, adipose depots provide feedback on hunger and dietary needs to the central nervous system. A variety of biochemical, physiological, and food-regulated mechanisms that alter abdominal obesity and thus disease risk are reviewed. Maeda identifies glucagon-like peptide 1 as an agonist of visceral fat adiposity and appetite. Castonguay defines the role of fructose in hypertriglyceridemia and obesity. Dietary foods play key roles in visceral fat accumulation and its removal. The effects of intermittent fasting versus daily calorie restriction on visceral fat loss are compared by Trepanowski and Varady. Laurant and colleagues show that gender and exercise, which both modulate cytokines, affect obesity and thus heart disease. Stress-induced eating also affects obesity, and Finch and Tomiyama describe relevant physiological and behavioral stress responses. Campbell and coworkers review fructose-induced hypertriglyceridemia as a cause of abdominal obesity that can be modified by changes in food intake. Yoshinaga describes how the gender and lifestyle of individuals and their parents combine to modify obesity.
Adipose tissues play important roles in health; their primary role is as a reserve of lipids needed to provide energy. Fat tissues consist of about 86% fat, and a variety of different cell types regulate fat accumulation. Lipolysis is modulated by lipolytic β-adrenergic receptors and antilipolysis is regulated by α2A adrenergic receptors. Dietary foods and supplements can play critical roles in modifying and preventing such fat accumulation. Park describes several types of soy protein and fermented soypastes that can reduce visceral obesity. Reviews by the Pimentel and Bautista-Castaño groups describe the roles of alcohol, coffee, and bread in modifying obesity through various mechanisms, including immunomodulation of inflammation, which is obesity induced. As Nagai and Takatsu review in humans and Masternak in animal models, these mechanisms are important in metabolic disorders associated with chronic diseases. Castonguay and coauthors describe appetite and reward signals in the brain, with sugar being a major mediator, as shown by magnetic resonance imaging.
Additionally, the effects of dietary supplements on fat regulation and thus visceral obesity are an important focus of this book. A stringent vegan diet with dietary restriction produces significant weight loss. A supplement containing flaxseed components changes visceral obesity, inflammation, lipids, and chronic hypertension, as Park summarizes. Damms-Machado shows that nutritional deficiencies in obese patients are a common condition, which are additionally impacted by bariatric operations, like sleeve gastrectomy. Miyashita and Hosokawa show the importance of plant carotenoids as nutraceutical therapies for visceral obesity.
Other macromolecules and foods are modulators of visceral fat and play a key role in a host of diseases, including diabetes, insulin resistance, cardiovascular disease, inflammation, and other obesity-related health problems. Pal and coauthors describe a role for psyllium as a therapy for obesity comorbidities. Karl and McKeown describe the role of whole grain (with its intrinsic fiber) in obesity prevention, while Pal defines a similar role for dietary whey protein. Vajro and coworkers describe the role of other complex carbohydrates known as probiotics in treating hepatic obesity and related diseases. Dinner carbohydrates, if used as described by Madar and colleagues, produce weight loss and have other effects on visceral fat. Citrus is a food that, as Mukai describes in animal models and humans, changes visceral fat accumulation. Lipids are the major modulators of fat. Tan describes the effects of dietary fatty acids on weight, fat mass and abdominal fat. Park shows that conjugated linoleic acid benefits human health by controlling weight. Finally, D’Antona reviews the current evidence that amino acid supplementation affects obesity. Free fatty acids are released from lipoproteins by enzymes and enter adipocytes to be reassembled into triglycerides for storage. Through regulating adipose tissues in visceral fat, different cell types (primarily adipocytes, fibroblasts, macrophages, lymphocytes, and endothelial cells) can have wide-ranging effects on health. Matikainen describes the role of fibroblast growth factor 21 in regulating energy metabolism in adipose tissues to promote health. Qi discusses how polymorphisms in the gene encoding neuropeptide Y (and other genes) affect central obesity. Finally, Garaulet defines site-specific adipose tissue fatty acid composition and its role in the regulation of abdominal obesity.
In conclusion, the authors describe how factors that affect the current abdominal obesity epidemic will provide major benefits by preventing chronic diseases, especially heart, vascular, and diabetic diseases. A broad range of disciplines are involved in dealing with the consequences of excessive abdominal fat, including cardiology, diabetes research, endocrinology, exercise physiology, and studies focusing on lipids, metabolism, nutrition, and obesity. We describe how abdominal obesity, a major cause of mortality and morbidity in much of the world through its associated diseases, can be regulated by food and dietary therapies.
Acknowledgments
The work of Dr. Watson’s editorial assistant, Bethany L. Stevens, and the project managers, Megan Wickline and Jeffrey Rossetti, in communicating with authors and working on the manuscripts was critical to the successful completion of the book. It is very much appreciated. Support for the work of Ms. Stevens and Dr. Watson was graciously provided by the Natural Health Research Institute (
), an independent, nonprofit organization that supports science-based research into natural health and wellness. It is committed to promoting scientific evidence for the usefulness and cost-effectiveness of diet, supplements, and a healthy lifestyle in improving health and wellness, and reducing disease. Finally, the work of Mari Stoddard, the librarian of the Arizona Health Science Library, was vital and very helpful in identifying key researchers who participated in the book.
Contributors
Machiko Aoki, MD, PhD Department of Pediatrics, Aoki Clinic of Internal Medicine, Cardiovascular Medicine & Pediatrics, Fukuoka, Japan.
Inmaculada Bautista-Castaño, MD, PhD Department of Clinical Sciences, University of Las Palmas de Gran Canaria, Las Palmas de Gran Canaria, Spain Biomedical Research Center Network on Obesity and Nutrition (CIBERobn) Physiopathology of Obesity and Nutrition, Institute of Health Carlos III, Madrid, Spain.
Paolo Bertassello, MD Division of Geriatric Medicine, University of Verona, Ospedale Maggiore, Verona, Italy.
Stephan C. Bischoff, MD, Prof. Institute of Nutritional Medicine, University of Hohenheim, Stuttgart, Germany.
Rafael Calpena, MD, PhD Department of Surgery, Bariatric Surgery Unit, General University Hospital Elche, Alicante, Spain.
Eric Campbell Department of Nutrition and Food Science, University of Maryland, College Park, MD, USA.
Raquel Canuto, PhD
Department of Nutrition, University of Vale do Rios dos Sinos, RS, Brazil.
Department of Nutrition, University of Caxias do Sul, RS, Brazil.
Thomas W. Castonguay, PhD Department of Nutrition and Food Science, University of Maryland, College Park, MD, USA.
Karine Clément, MD, PhD Institute of Cardiometabolism and Nutrition, ICAN, Pitié-Salpêtrière Hospital; Assistance Publique-Hôpitaux de Paris, CRNH-Ile de France, Paris, France.
Anderson da Silva Garcez, MD Postgraduate Program in Collective Health, University of Vale do Rios dos Sinos, RS, Brazil.
Antje Damms-Machado, PhD Institute of Nutritional Medicine, University of Hohenheim, Stuttgart, Germany.
Roberta D’Aniello, MD Department of Medicine and Surgery, Medical School of Salerno, Baronissi, Salerno, Italy.
Giuseppe D’Antona, MD, PhD Department of Molecular Medicine and the Laboratory for the Study of Motor Activities in Rare Diseases, University of Pavia, Voghera, Italy.
Sylwia Dzięgielewska-Gęsiak Department of Internal Diseases, Silesian Medical University, Katowice, Poland.
Magdy El-Salhy, MD, PhD
Section for Gastroenterology, Department of Medicine, Stord Helse-Fonna Hospital, Norway.
Section for Gastroenterology, Department of Clinical Medicine, University of Bergen, Norway.
Francesco Fantin, MD, PhD Division of Geriatric Medicine, University of Verona, Ospedale Maggiore, Verona, Italy.
Laura E. Finch, B.S. Cornell University Department of Psychology, Los Angeles, CA, USA.
Carmine Finelli, MD, PhD INT Fondazione Pascale
- Cancer Research Center of Mercogliano, Mercogliano (AV), Italy.
Gershon Fink, MD Kaplan Medical Center, Rehovot, Israel.
Yuya Fujishima, MD Department of Metabolic Medicine, Graduate School of Medicine, Osaka University, Osaka, Japan.
Marta Garaulet, PhD, Full Professor of Physiology, Department of Physiology, Faculty of Biology, University of Murcia, Murcia, Spain.
Danijela Gasevic, MD Department of Biomedical Physiology and Kinesiology, Simon Fraser University, Burnaby, British Columbia, Canada.
Eliana Geller Department of Nutrition and Food Science, University of Maryland, College Park, MD, USA.
Sonia Gómez-Martínez, PhD, Research officer Department of Metabolism and Nutrition, Institute of Food Science, Technology and Nutrition, Spanish National Research Council, Madrid, Spain.
Doris Gundersen, PhD Department of Research, Helse-Fonna, Haugesund, Norway.
Martin Hagger School of Public Health; Curtin Health Innovation Research Institute; Curtin University of Technology, Perth, Western Australia, Australia.
Takashi Hamajima, MD Department of Endocrinology and Metabolism, Aichi Children’s Health and Medical Center, Motiokamachi, Obu, Aichi, Japan.
Jan Gunnar Hatlebakk, MD, PhD
Section for Gastroenterology, Department of Clinical Medicine, University of Bergen, Norway.
Section for Gastroenterology, Department of Medicine, Haukland University Hospital, Bergen, Norway.
Trygve Hausken, MD, PhD
Section for Gastroenterology, Department of Clinical Medicine, University of Bergen, Norway.
Section for Gastroenterology, Department of Medicine, Haukland University Hospital, Bergen, Norway.
Suleen Ho, PhD, Hons School of Public Health, Curtin Health Innovation Research Institute, Curtin University of Technology, Perth, Western Australia, Australia.
Lyndsey M. Hornbuckle, PhD, RD Department of Exercise Science and Sport Management, Kennesaw State University, Kennesaw, Georgia, USA.
Masashi Hosokawa Faculty of Fisheries Sciences, Hokkaido University, Hakodate, Japan.
Samantha M. Hudgins Department of Nutrition and Food Science, University of Maryland, College Park, MD, USA.
Gary R. Hunter, PhD Department of Human Studies, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Monica Jane, BSc School of Public Health, Curtin Health Innovation Research Institute, Curtin University of Technology, Perth, Western Australia, Australia.
J. Philip Karl, MS, RD Jean Mayer USDA Human Nutrition Research Center on Aging, Tufts University, Boson, MA, USA.
Nadia Khan MD, MSc Department of Medicine, University of British Columbia, Vancouver, British Columbia, Canada.
Simi Kohli, MD, MSc Department of Biomedical Physiology and Kinesiology, Simon Fraser University, Burnaby, British Columbia, Canada.
Teresa Kokot, MD, PhD Department of Internal Diseases, Silesian Medical University, Katowice, Poland.
Pascal Laurant, PhD Laboratoire Pharm-Ecologie Cardiovasculaire, UFRip Sciences Technologies Santé, Université d’Avignon et des Pays du Vaucluse, Avignon, France.
Scott A. Lear, PhD Faculty of Health Sciences, Simon Fraser University, Vancouver, British Columbia, Canada.
Marie-Ève Leblanc, RN, MSc Faculty of Pharmacy, Université Laval and Institut Universitaire de Cardiologie et de Pneumologie de Québec, Quebec City, Quebec, Canada.
Myoungsook Lee, PhD Department of Food and Nutrition, and Research Institute of Obesity Sciences, Sungshin Women’s University, Seoul, Korea.
Zecharia Madar Kaplan Medical Center, Rehovot, Israel.
Norikazu Maeda, MD, PhD Department of Metabolic Medicine, Graduate School of Medicine, Osaka University, Osaka, Japan.
Ascensión Marcos Department of Metabolism and Nutrition, Institute of Food Science, Technology and Nutrition, Spanish National Research Council, Madrid, Spain.
David Martínez-Gómez, PhD, Associate lecturer Department of Physical Education, Sports and Human Movement, Faculty of Teacher Training and Education, Universidad Autónoma de Madrid, Madrid, Spain.
Grazia Massa, RD Department of Medicine and Surgery, Medical School of Salerno, Baronissi, Salerno, Italy.
Michal M. Masternak, PhD University of Central Florida, Burnett School of Biomedical Sciences, College of Medicine, Orlando, FL, USA.
Niina Matikainen, MD, PhD Department of Endocrinology and Cardiovascular Research Unit, Heart and Lung Center, Helsinki University Central Hospital, University of Helsinki, Helsinki, Finland.
Michele L. McCarroll, PhD Department of Obstetrics and Gynecology, Summa Health System, Akron, Ohio, USA.
Jenny-Lee McKay, BSc School of Public Health, Curtin Health Innovation Research Institute, Curtin University of Technology, Perth, Western Australia, Australia.
Nicola M. McKeown, PhD Jean Mayer USDA Human Nutrition Research Center on Aging, Tufts University, Boson, MA, USA.
Thayana O. Micheletti Department of Internal Medicine, Faculty of Medical Sciences, University of Campinas (UNICAMP), São Paulo, Brazil.
Kazuo Miyashita Faculty of Fisheries Sciences, Hokkaido University, Hakodate, Japan.
Ayumi Miyazaki, MD, PhD Department of Pediatrics, Japan Community Health Care Organization Takaoka-Fushiki Hospital, Takaoka, Toyama, Japan.
Małgorzata Muc-Wierzgoń Department of Internal Diseases, Silesian Medical University, Katowice, Poland.
Katsuyuki Mukai R&D Center, UNITIKA Ltd, Uji, Kyoto, Japan.
Yoshinori Nagai, MD, PhD, FAHA Department of Immunobiology and Pharmacological Genetics, Graduate School of Medicine and Pharmaceutical Science for Research, University of Toyama, Toyama-shi, Toyama, Japan.
Masami Nagashima, MD, PhD, FAHA Department of Rehabilitation, Aichi Saiseikai Rehabilitation Hospital, Nishi-ku, Nagoya, Japan.
Astrid Nehlig French Medical Research Institute, INSERM U 663, Faculty of Medicine, Strasbourg, France.
Ewa Nowakowska-Zajdel Department of Internal Diseases, Silesian Medical University, Katowice, Poland.
Maria Teresa Anselmo Olinto, PhD
Postgraduate Program in Collective Health, University of Vale do Rios dos Sinos, RS, Brazil.
Department of Nutrition, Federal University of Health Science of Porto Alegre, RS, Brazil.
Sebely Pal, PhD, Hons School of Public Health, Curtin Health Innovation Research Institute, Curtin University of Technology, Perth, Western Australia, Australia.
Giulia Paolella, MD Department of Medicine and Surgery, Medical School of Salerno, Baronissi, Salerno, Italy.
Jae B. Park Diet, Genomics, and Immunology Laboratory, Beltsville Human Nutrition Research Center, United States Department of Agriculture Agricultural Research Service, Beltsville, MD, USA.
Yeonhwa Park Department of Food Science, University of Massachusetts, Amherst, MA, USA.
Yongsoon Park, PhD Department of Food and Nutrition, Hanyang University, Seoul, Korea.
Zdenka Pausova, MD The Hospital for Sick Children, University of Toronto, Toronto, Canada.
Fátima Pérez de Heredia, PhD Lecturer in Physiology, School of Natural Sciences and Psychology, Liverpool John Moores University, Liverpool, United Kingdom.
Luca Pierri, MS Department of Medicine and Surgery, Medical School of Salerno, Baronissi, Salerno, Italy.
Gustavo D. Pimentel Department of Internal Medicine, Faculty of Medical Sciences, University of Campinas (UNICAMP), São Paulo, Brazil.
Cristina Pizza, MS Department of Medicine and Surgery, Medical School of Salerno, Baronissi, Salerno, Italy.
Marco Poeta, MS Department of Medicine and Surgery, Medical School of Salerno, Baronissi, Salerno, Italy.
Paul Poirier, MD, PhD, FRCPC, FACC, FAHA Faculty of Pharmacy, Université Laval and Institut Universitaire de Cardiologie et de Pneumologie de Québec, Quebec City, Quebec, Canada.
Christine Poitou, MD, PhD Institute of Cardiometabolism and Nutrition, ICAN, Pitié-Salpêtrière Hospital; Assistance Publique-Hôpitaux de Paris, CRNH-Ile de France, Paris, France.
Lu Qi, MD, PhD
Department of Nutrition, Harvard School of Public Health, Boston, MA, USA.
Channing Division of Network Medicine, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, USA.
Simone Radavelli-Bagatini, PhD, Hons School of Public Health, Curtin Health Innovation Research Institute, Curtin University of Technology, Perth, Western Australia, Australia.
Catherine Riva, PhD Laboratoire Pharm-Ecologie Cardiovasculaire, UFRip Sciences Technologies Santé, Université d’Avignon et des Pays du Vaucluse, Avignon, France.
Andrea P. Rossi, MD, PhD Division of Geriatric Medicine, University of Verona, Ospedale Maggiore, Verona, Italy.
G. Dante Roulette, MD Department of Obstetrics and Gynecology, Summa Health System, Akron, Ohio, USA.
Jaime Ruiz-Tovar, MD, PhD Department of Surgery, Bariatric Surgery Unit, General University Hospital Elche, Alicante, Spain.
Almudena Sanchez-Villegas DPharm, PhD Department of Clinical Sciences, University of Las Palmas de Gran Canaria, Las Palmas de Gran Canaria, Spain Biomedical Research Center Network on Obesity and Nutrition (CIBERobn) Physiopathology of Obesity and Nutrition, Institute of Health Carlos III, Madrid, Spain.
Maria Sangermano, MD Department of Medicine and Surgery, Medical School of Salerno, Baronissi, Salerno, Italy.
E. Sartori, MD Division of Geriatric Medicine, University of Verona, Ospedale Maggiore, Verona, Italy.
Anna Schlappal, PhD Department of Nutrition and Food Science, University of Maryland, College Park, MD, USA.
Luis Serra-Majem MD, PhD Department of Clinical Sciences, University of Las Palmas de Gran Canaria, Las Palmas de Gran Canaria, Spain Biomedical Research Center Network on Obesity and Nutrition (CIBERobn) Physiopathology of Obesity and Nutrition, Institute of Health Carlos III, Madrid, Spain.
Masaki Shinomiya, MD, PhD Department of Internal Medicine, Nishifuna Naika, Funabashi, Chiba, Japan.
Sigal Sofer, MSc, RD Institute of Biochemistry, Food Science and Nutrition, The Robert H. Smith Faculty of Agriculture, Food and Environment, The Hebrew University of Jerusalem, Jerusalem, Israel.
Aliza Stark, PhD, RD Institute of Biochemistry, Food Science and Nutrition, The Robert H. Smith Faculty of Agriculture, Food and Environment, The Hebrew University of Jerusalem, Jerusalem, Israel.
Edyta Suliga, PhD Department of the Prevention of Alimentary Tract Diseases, Faculty of Health Sciences, Jan Kochanowski University, Kielce, Poland.
Kiyoshi Takatsu, PhD Toyama Prefectural Institute for Pharmaceutical Research, Imizu City, Toyama, Japan.
Katsuhiko Takayanagi R&D Center, UNITIKA Ltd, Uji, Kyoto, Japan.
Sze Yen Tan, PhD, APD University of South Australia, School of Pharmacy and Medical Sciences, Adelaide, Australia.
Giovanni Tarantino, MD Department of Clinical Medicine and Surgery, Federico II University Medical School of Naples, Naples, Italy and INT Fondazione Pascale
- Cancer Research Center of Mercogliano, Mercogliano (AV), Italy.
A. Janet Tomiyama, PhD Department of Psychology, University of California, Los Angeles, CA, USA.
John F. Trepanowski, MS Department of Kinesiology and Nutrition, University of Illinois, Chicago, Chicago, IL, USA.
Pietro Vajro, MD
Department of Medicine and Surgery, Medical School of Salerno, Baronissi, Salerno, Italy.
European Laboratory for the Investigation of Food-Induced Diseases, University of Naples Federico II, Naples, Italy.
Krista Varady, PhD Department of Kinesiology and Nutrition, University of Illinois, Chicago, Chicago, IL, USA.
Camille Vatier, MD Institute of Cardiometabolism and Nutrition, ICAN, Pitié-Salpêtrière Hospital; Assistance Publique-Hôpitaux de Paris, CRNH-Ile de France, Paris, France.
Agnes Vinet, PhD Laboratoire Pharm-Ecologie Cardiovasculaire, UFRip Sciences Technologies Santé, Université d’Avignon et des Pays du Vaucluse, Avignon, France.
Vivian E. von Gruenigen, MD Department of Obstetrics and Gynecology, Summa Health System, Akron, Ohio, USA.
Min Xu, MD, PhD
Department of Nutrition, Harvard School of Public Health, Boston, MA, USA.
Shanghai Clinical Center for Endocrine and Metabolic Diseases, Shanghai Institute of Endocrine and Metabolic Diseases, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Masao Yoshinaga, MD, PhD Department of Pediatrics, National Hospital Organization Kagoshima Medical Center, Kagoshima, Japan.
Mauro Zamboni, MD Division of Geriatric Medicine, University of Verona, Ospedale Maggiore, Verona, Italy.
Valeria Zanandrea, MD Division of Geriatric Medicine, University of Verona, Ospedale Maggiore, Verona, Italy.
Section 1: Epidemiology and Clinical Management of Visceral Obesity
Part 1: Epidemiology and Pathophysiology of Abdominal Obesity
Outline
Diet and Irritable Bowel Syndrome, with a Focus on Appetite-Regulating Gut Hormones
Work and Abdominal Obesity Risk
Effects of Dietary Patterns and Physical Activity on the Establishment of Abdominal Obesity in Adolescents
Lifestyle Factors Affecting Abdominal Obesity in Children and Adolescents Risks and Benefits
Female Cancer Survivorship and Obesity
Evaluation of Visceral Fat in Massive Obesity
Beyond Nutrition Is There Any Role for Physical Activity in Nonalcoholic Fatty Liver Disease Therapy?
Abdominal Fat and African-Americans Incidence and Relationship to Disease
Chapter 1
Diet and Irritable Bowel Syndrome, with a Focus on Appetite-Regulating Gut Hormones
Magdy El-Salhya, c, Doris Gundersenb, Jan Gunnar Hatlebakkc and Trygve Hauskenc, aSection for Gastroenterology, Department of Medicine, Stord Helse-Fonna Hospital, Norway, bDepartment of Research, Helse-Fonna, Haugesund, Norway, cSection for Gastroenterology, Institute of Medicine, University of Bergen, Norway
Abstract
Irritable bowel syndrome (IBS) is a common gastrointestinal disorder with a prevalence of 5–20% and an incidence of 200/100,000. It is not known to be associated with the development of serious disease or with increased mortality, but it does considerably reduce the quality of life for patients and is an economic burden to society. Diet plays an important role in triggering the symptoms of IBS, especially the intake of foods that are rich in fermentable oligo-, di-, and monosaccharides, and polyols (FODMAPs), by influencing the dominance of Clostridium spp. in the intestinal flora and inducing abnormalities in gut endocrine cells. Dietary guidance aimed at establishing healthy eating habits by avoiding foods rich in FODMAPs and insoluble fiber and adjusting food composition has been found to reduce symptoms and improve the quality of life in IBS patients. Endocrine cells that produce several anorexigenic hormones in the gut are depleted in IBS patients, but the impact of this on appetite and body mass index in IBS patients is not known. Further studies are urgently needed to clarify this issue.
Keywords
Appetite
Cholecystokinin
Diet
Enteroglucagon
Irritable bowel syndrome
Ghrelin
Motility
Peptide YY
Visceral hypersensitivity
Introduction
Irritable bowel syndrome (IBS) is a common chronic gastrointestinal disorder with a prevalence of 5–20% and a reported incidence of 200 cases per 100,000 in the adult population [1–9]. IBS patients are often young and predominantly female, and IBS is associated with abnormal gastrointestinal motility and visceral hypersensitivity [2,6,10–25]. Patients with IBS complain of abdominal pain or discomfort, altered bowel habits, and bloating and/or abdominal distension [1]. The severity of symptoms varies from tolerable to severe, with some patients suffering from daily symptoms while others report intermittent symptoms at intervals of weeks or months [1].
Although IBS is not known to be associated with the development of serious disease or increased mortality, it does considerably reduce the patients quality of life by an amount comparable to that reported for patients with inflammatory bowel disease, diabetes, congestive heart failure, renal insufficiency, and hepatic cirrhosis [1,6,26–31]. In addition to the morbidity caused by IBS, this disorder represents an economic burden to society [1]. Although most IBS patients ignore their symptoms and regard them as a normal part of everyday life, they generate a substantial workload in both primary and secondary health care [32,33]. It has been reported that IBS patients are responsible for 12–14% of primary health-care visits and constitute 28% of referrals to gastroenterologists [34–43]. Added to this are the costs associated with diagnostic tests, medication, hospitalization, and the reduced productivity of IBS patients [36,41,42].
IBS diagnosis is based mainly on symptom assessment since there are no biochemical, radiological, or morphological diagnostic tests for the condition. The Rome criteria III are widely accepted and applied for the diagnosis of IBS [44]. Patients are subdivided further on the basis of differences in the predominant bowel pattern into diarrhea predominant (IBS-D), constipation predominant (IBS-C), or a mixture of both diarrhea and constipation (IBS-M). These three subtypes have a similar prevalence [34,45–49]. Although several biomarkers for the diagnosis of IBS have been considered, the only reproducible test is gut transit measured by radioisotope markers, and this test has a limited availability [50]. Duodenal chromogranin A cell density has been proposed as a good marker for the diagnosis of IBS, with high sensitivity and specificity, but needs to be confirmed in a large cohort of IBS patients [51]. Postinfectious IBS is a subset of IBS that occurs in a considerable number of patients and is defined as a sudden onset of IBS symptoms following gastroenteritis in individuals who have not previously had any gastrointestinal complaints [52]. However, postinfectious IBS has also been reported following nongastrointestinal infections such as respiratory, urinary tract, and skin infections [53]. It is reported that 6–17% of IBS patients believe that their symptoms began with an infective illness, and 7–31% of patients who suffer an acute episode of infectious gastroenteritis go on to develop postinfectious IBS despite clearance of the inciting pathogen [54–56].
There are both nonpharmacological and pharmacological options for the treatment of IBS. The nonpharmacological approach comprises the provision of information, reassurance, dietary guidance, regular exercise, probiotic intake, gut-directed hypnotherapy, cognitive therapy, acupuncture, and herbal therapy. Pharmacological treatment depends upon the symptoms and mainly includes antidiarrheal drugs, prokinetics, laxatives, antispasmodics, antidepressants, antianxiety drugs, and antibiotics [1].
Diet Intake in Irritable Bowel Syndrome Patients
IBS patients tend to avoid certain food items that they associate with onset of their symptoms such as milk and dairy products, wheat products, caffeine, certain meat, cabbage, onion, peas/beans, hot spices, fried food, and smoked food products [57,58]. It has been reported that 62% of IBS patients limit or exclude food items from their daily intake, with 12% of them making such drastic changes to their diet that long-term nutritional deficiencies are possible [59]. Despite such food avoidance, the dietary composition of IBS patients does not differ from the background population in terms of energy, carbohydrate, protein, and fat intake [60–66]. A common belief among IBS patients is that lactose is the main cause of their symptoms; they consequently reduce their intake of milk and dairy products, which in turn results in a low daily intake of calcium, vitamin B2, and phosphorus [59,63,65,67].
IBS patients have a lower consumption of food items known to be rich in fermentable oligo-, di-, and monosaccharides, and polyols (i.e. FODMAPs) such as buns, couscous, millet, pasta, spaghetti, rice, and some vegetables (e.g. raw broccoli, cabbage, garlic, green beans, leeks, mushrooms, onion, peppers, and tomatoes) [63]. However, they have a higher consumption of other FODMAP-rich vegetables such as grapes, mango, melon, peaches, pears, peas, and plums [63].
The Role of Diet in the Development of IBS Symptoms
Food Allergy or Intolerance
There is no convincing evidence for an allergic response to, or an intolerance for, any specific foodstuff in IBS [1,68–73]. In absence of a typical immunoglobulin E (IgE) reaction, another antibody class (IgG) has been suggested to be implicated in food-related allergies in IBS [74,75]. However, this suggestion is controversial, probably because the tests used are not sufficiently sensitive or specific [65,68,73,75–83]. Nevertheless, food allergy mediated by mucosal mechanisms may occur in patients with atopic and postinfectious IBS [1,55,84].
The triggering of IBS symptoms by the ingestion of wheat products is thought to be caused by the sugar polymers, fructans and galactans [85,86],. The occurrence of nonceliac gluten sensitivity in IBS patients is widely debated [87]. The existence of nonceliac gluten intolerance was advocated following a randomized, double-blind, placebo-controlled rechallenge trial [88]. It has been suggested that IBS patients with wheat intolerance who possess genotypes associated with celiac disease (HLA DQ2 or DR3) but do not have typical serological markers or changes in small intestine histology exhibit other immunologic evidence of gluten reactivity and respond to a gluten-free diet [89]. The role of gluten intolerance in IBS remains to be clarified. Celiac disease and IBS have overlapping clinical presentations, resulting in some patients with celiac disease being mistakenly diagnosed as having IBS [90,91]. The number of patients with celiac disease among those with IBS is reported to vary between 0.04% and 4.7% [92–102].
Poorly Absorbed Carbohydrates and Fibers
FODMAPs are short-chain carbohydrates that are poorly absorbed, and a significant portion of these ingested carbohydrates enter the distal small bowel and colon [103]. These sugars include fructose, lactose, sugar alcohols (sorbitol, maltitol, mannitol, xylitol, and isomalt), fructans, and galactans. Fructose and lactose are present in apples, pears, watermelon, honey, fruit juices, dried fruits, and milk and milk products. Polyols are used in low-calorie food products. Galactans and fructans are present in wheat, rye, artichokes, asparagus, broccoli and Brussels sprouts, cabbage, garlic, leeks, onions, legumes, lentils, and soy [90,91,104].
FODMAPs increase the osmotic pressure within the large intestine and provide a substrate for bacteria fermentation, leading to gas production and distension of the large intestine. An increase in the intraluminal pressure can stimulate the release of serotonin and substance P into the interstitial fluid. Serotonin activates the submucosal sensory branch of the enteric nervous system (ENS), which conveys the sensation to the central nervous system (CNS), probably causing abdominal pain and discomfort [105–107]. Furthermore, serotonin controls gastrointestinal motility and chloride secretion via interneurons and motor neurons, which may result in motility and secretion disturbances [105–107]. Although increasing dietary fiber intake is still recommended for patients with IBS, especially those with IBS-C, clinical practice shows that this increases abdominal pain, bloating, and distension [108]. However, it has been shown that soluble fiber intake is effective in improving overall IBS symptoms and has fewer side effects than insoluble fiber [44–46,109–111].
The fermentation of FODMAPs and insoluble fiber to produce gas and intraluminal distention depends upon the composition of the intestinal flora. A dominance of Clostridium spp. in the intestinal flora over beneficial bacteria such as Lactobacillus and Bifidobacterium spp., which do not produce gas upon fermenting carbohydrates, would worsen the IBS symptoms [1]. On the other hand, consuming foods supplemented with probiotics that contain these latter bacteria would increase tolerance to both FODMAPs and fiber [1].
Abnormalities in the Endocrine System of the Gut in Irritable Bowel Syndrome
The Endocrine System of the Gut
The field of endocrinology originated in 1902 following the discovery of secretin by Bayliss and Starling [112,113]. Despite the dominance of the concept of nervism in controlling the gut function, which was introduced by Pavlov in the nineteenth century, it has now been established that the gut is an endocrine organ that controls its own function [114]. This was possible due to the development of novel techniques for the isolation, purification, and measurement of a large number of recently discovered gut hormones [115]. It is currently believed that the gut is controlled by a complicated integrated mechanism that includes both endocrine and nervous components, which interact with each other [1]. This regulatory system—which lies within the gut and communicates with the CNS—is called the neuroendocrine system (NES) of the gut [1,107].
The gut NES is a local regulatory system that controls the primary gut functions (i.e. the digestion and absorption of nutrients) by regulating gut motility, secretion, absorption, microcirculation, local immune defense, and cell proliferation [1,107]. Moreover, to optimize the digestion and absorption processes, the gut NES regulates appetite and the secretion of many gut hormones in order to reduce food intake and limit meal size [115].
The NES of the gut consists of two parts: (1) endocrine cells that are spread between the epithelial cells of the mucosa facing the gut lumen; and (2) peptidergic and serotonergic as well as nitric oxide-containing nerves of the ENS in the gut wall. The NES of the gut comprises a large number of bioactive messengers that act via endocrine, paracrine, or neuroendocrine pathways, or by synaptic signaling. The different components of this system interact and are integrated both with each other and with the afferent and efferent nerve fibers of the CNS [1]. The gut intraluminal content of carbohydrates, proteins, or fat triggers the release of different signaling substance of the NES of the gut (Fig. 1.1) [1,107].
Figure 1.1 Schematic drawing of triggering the release of different gut hormones by the intraluminal of nutrient content. Depending upon the intraluminal content of proteins, carbohydrates, or fat, a particular gut hormone is released into the interstitial fluid, where it may act via endocrine/paracrine action or as a neurotransmitters/neuromodulators on the neurons in the enteric nervous system. CCK, cholecystokinin; GIP, gastric inhibitory polypeptide; NPY, neuropeptide Y; PP, pancreatic polypeptide; PYY, peptide YY.
Abnormalities in Gut Endocrine Cells in Patients with Irritable Bowel Syndrome
There seems to be a general depletion of gut endocrine cells in patients with sporadic IBS [51,116,117]. Several abnormalities in the density of gut endocrine cells have been described in both sporadic and postinfectious IBS patients (Tables 1.1 and 1.2) [55,118–132]. It is noteworthy that the abnormalities observed are structural and not merely changes in hormone concentration. Changes in hormone levels reflect hormone synthesis and release in response to a physiologic condition, while structural changes represent a longstanding condition with long-term consequences. The abnormalities listed in Table 1.1 may explain the abnormal gastrointestinal secretion, motility, and visceral hypersensitivity seen in patients with IBS.
Table 1.1
Abnormalities in Gut Endocrine Cells in Patients with Sporadic Irritable Bowel Syndrome
IBS-C, irritable bowel syndrome, constipation predominant; IBS-D, irritable bowel syndrome, diarrhea predominant.
Table 1.2
Abnormalities in the Gut Endocrine Cell Densities in Patients with Postinfectious Irritable Bowel Syndrome
Irritable Bowel Syndrome and Appetite-Regulating Gut Hormones
Appetite regulation is complex and involves a large number of peptide hormones, several of which are gut hormones [115]. Many gut hormones act on the hypothalamic centers of appetite control [115]. The arcuate nucleus (ARC), which acts as the center for integrating neurological and blood-borne signals, lies in the median eminence. This region lacks a complete blood-brain barrier and is thus susceptible to factors circulating in the blood [133–135]. Similarly, the brainstem is proximal to other regions with an incomplete blood-brain barrier, allowing it to receive blood-borne signals [115,135]. The intake of palatable foods (hedonic feeding) is controlled by the brain reward system in the midbrain, which is modulated by blood-borne signals [135].
The function of five hormones known to be involved in appetite regulation are altered in the gut of IBS patients: ghrelin, cholecystokinin (CCK), peptide YY (PYY), enteroglucagon (oxyntomodulin), and serotonin. Ghrelin is an orexigenic hormone, while CCK, PYY, enteroglucagon, and serotonin are anorexigenic hormones.
Ghrelin is a 28-amino-acid peptide hormone that was first isolated from the stomach [124,136–138]. The major source of circulating ghrelin is endocrine cells of the oxyntic mucosa of the stomach, but small amounts are expressed in the small intestine, the large intestine, and the ARC of the hypothalamus [136–139]. Ghrelin has several functions, including regulating the release of somatotropin/growth hormone (GH) from the pituitary gland, where it acts synergistically with the GH-releasing hormone [136–139]. Moreover, ghrelin accelerates gastric and intestinal motility [140–153]. Ghrelin also increases appetite and feeding and plays a major role in energy metabolism [115,135]. Thus, both central and peripheral administration of ghrelin stimulates food intake and body weight gain [136]. Ghrelin is involved in meal initiation: ghrelin plasma levels rise during fasting and fall upon eating, and are inversely correlated with body weight. Moreover, basal ghrelin levels rise after weight loss [154–164]. As mentioned above, patients with IBS-D have a high density of ghrelin-producing cells, while in IBS-C the density of these cells is low (Fig. 1.2) [118]. However, the plasma ghrelin level in these patients does not appear to differ from that of healthy controls [118,119,165]. It has been postulated that the change in the number of ghrelin units (cells) is compensated by a change in synthesis and/or release of this hormone and that symptoms develop when there is fatigue in this compensation mechanism [118]. This change in ghrelin implies an increase in appetite and food intake in IBS-D, and a corresponding decrease in IBS-C.
Figure 1.2 Ghrelin-immunoreactive cells in the oxyntic mucosa of a healthy subject (A), a patient with irritable bowel syndrome, diarrhea predominant (B) and a patient with irritable bowel syndrome, constipation predominant (C).
In addition to the functions of CCK shown in Table 1.1, this hormone has an anorexigenic action [166–177]. There are two receptors for CCK: CCK-A and CCK-B (or CCK-1 and CCK-2, respectively) [178–182]. Both receptor subtypes are distributed throughout the CNS and gut, although CCK-A receptors predominate in the gut and CCK-B receptors predominate in the brain [178–182]. The density of duodenal CCK cells is reported to be reduced in sporadic IBS (Fig. 1.3) and increased in postinfectious IBS [120,121]. An increase in food intake in sporadic IBS and decreased food intake in postinfectious IBS is therefore to be expected.
Figure 1.3 Cholecystokinin-producing cells in the duodenum of a healthy subject (A) and a patient with irritable bowel syndrome (B).
PYY is released into the circulation following a meal in proportion to the calories ingested and the meal composition [183]. Infusion of PYY3-36 reduced food consumption during test meals, and obese subjects had a low PYY plasma level [184,185]. Circulating PYY3-36 binds to Y2 receptors on the presynaptic terminals of hypothalamic neuropeptide Y (NPY) and agouti-related protein (AgRP) neurons, and inactivation of these neurons is associated with the induction of anorexia [186]. PYY is a major regulator of the ileal brake in that it acts to inhibit further food intake once nutrients, and especially lipids, have reached the distal small intestine (ileum) [187–196]. The density of PYY cells is generally decreased in sporadic IBS (Table 1.1 and Fig. 1.4). However, whether this increases food intake and appetite in IBS patients remains to be established.
Figure 1.4 Peptide YY-immunoreactive cells in the colon of a healthy subject (A) and a patient with irritable bowel syndrome (B).
Enteroglucagon is released into the blood circulation following food ingestion in proportion to the amount of calories ingested [197,198]. It has some effect on incretin and reduces gastric motility and secretion [199–204]. However, enteroglucagon is considered to have only a modest anorexigenic effect [135]. Serotonin is also known to exert an anorexigenic effect [205]. The densities of enteroglucagon- and serotonin-producing cells are reduced in patients with IBS, which might have an impact on their food intake and appetite.
While several appetite-regulating gut hormones are altered in patients with IBS, body mass index (BMI) and appetite have not been studied in detail, and the few available data are controversial. Thus, while Simrén et al. reported that most of the 330 IBS patients they examined were normal or overweight, Kubo et al. found that low BMI was associated with IBS in the 367 patients they investigated [57,206]. It is noteworthy that several studies found that food intake in IBS patients did not differ from that of the normal control population [60–66]. It has yet to be determined whether IBS patients have increased appetite or whether the avoidance of eating because of worsening of symptoms upon eating prevents excessive food intake and therefore excessive weight gain. Further studies are needed to clarify this issue.
Effect of Dietary Guidance
Dietary guidance should include information regarding the importance of regular meals and healthy eating habits, the avoidance of dietary FOODMAPs, and the insoluble fiber content of the dietary components and to avoid them. This guidance should also include helping patients to identify the food items that they do not tolerate well [63,66]. the provision of dietary guidance to IBS patients resulted in the consumption of a better diet with respect to vitamins and minerals. In addition, patients were made aware of FODMAP-rich food items so that these could be avoided or consumed in low quantities, ultimately resulting in reduced symptoms and an improved quality of life [63]. Patients also consumed more food items supplemented with Lactobacillus and Bifidobacterium spp. which in turn increased their tolerance to FOODMAPs [63].
Conclusion
IBS is a common gastrointestinal disorder. Although it does not develop into a serious disease or increase mortality, it does considerably reduce the quality of life of the patients and is an economic burden to society. Diet plays an important role in the development of IBS symptoms. IBS symptoms can be caused by the intake of FODMAP-rich foods, the dominance of Clostridium spp. in the intestinal flora, and abnormalities in gut endocrine cells. Guidance aimed at establishing healthy eating habits, the avoidance of FODMAP-rich food and insoluble fiber, and adjusting the dietary composition reduces symptoms and improves the quality of life in IBS patients. Several of the endocrine cells that produce anorexigenic gut hormones are depleted in IBS patients. However, the possible impact on appetite and BMI in IBS patients is unknown; further studies are therefore urgently needed to clarify this issue.
References
1. El-Salhy M, Gundersen D, Hatlebakk JG, Hausken T. Irritable bowel syndrome: diagnosis, pathogenesis and treatment options. New York: Nova Science Publishers, Inc.; 2012
2. Ford AC, Vandvik PO. Irritable bowel syndrome. Clin Evid. 2012;01:410.
3. Quigley EM, Locke GR, Mueller-Lissner S, et al. Prevalence and management of abdominal cramping and pain: a multinational survey. Aliment Pharmacol Ther. 2006;24:411-419.
4. Vandvik PO, Lydersen S, Farup PG. Prevalence, comorbidity and impact of irritable bowel syndrome in Norway. Scand J Gastroenterol. 2006;41:650-656.
5. Drossman DA, Li Z, Andruzzi E, et al. U.S. householder survey of functional gastrointestinal disorders. Prevalence, sociodemography, and health impact. Dig Dis Sci. 1993;38:1569-1580.
6. Wong RK, Drossman DA, Weinland SR, et al. Partner burden in irritable bowel syndrome. Clin Gastroenterol Hepatol. 2013;11:151-155.
7. Saito YA, Schoenfeld P, Locke 3rd GR. The epidemiology of irritable bowel syndrome in North America: a systematic review. Am J Gastroenterol. 2002;97:1910-1915.
8. Locke 3rd GR, Yawn BP, Wollan PC, Melton 3rd LJ, Lydick E, Talley NJ. Incidence of a clinical diagnosis of the irritable bowel syndrome in a United States population. Aliment Pharmacol Ther. 2004;19:1025-1031.
9. Lovell RM, Ford AC. Global prevalence of and risk factors for irritable bowel syndrome: a meta-analysis. Clin Gastroenterol Hepatol. 2012;10:712-721.
10. Whorwell PJ, Clouter C, Smith CL. Oesophageal motility in the irritable bowel syndrome. BMJ. 1981;282:1101-1102.
11. Caballero-Plasencia AM, Valenzuela-Barranco M, Herrerias-Gutierrez JM, Esteban-Carretero JM. Altered gastric emptying in patients with irritable bowel syndrome. Eur J Nucl Med. 1999;26:404-409.
12. Evans PR, Bak YT, Shuter B, Hoschl R, Kellow JE. Gastroparesis and small bowel dysmotility in irritable bowel syndrome. Dig Dis Sci. 1997;42:2087-2093.
13. van Wijk HJ, Smout AJ, Akkermans LM, Roelofs JM, ten Thije OJ. Gastric emptying and dyspeptic symptoms in the irritable bowel syndrome. Scand J Gastroenterol. 1992;27:99-102.
14. Cann PA, Read NW, Brown C, Hobson N, Holdsworth CD. Irritable bowel syndrome: relationship of disorders in the transit of a single solid meal to symptom patterns. Gut. 1983;24(5):405-411.
15. Kellow JE, Phillips SF. Altered small bowel motility in irritable bowel syndrome is correlated with symptoms. Gastroenterology. 1987;92(6):1885-1893.
16. Kellow JE, Phillips SF, Miller LJ, Zinsmeister AR. Dysmotility of the small intestine in irritable bowel syndrome. Gut. 1988;29(9):1236-1243.
17. Mertz H, Naliboff B, Munakata J, Niazi N, Mayer EA. Altered rectal perception is a biological marker of patients with irritable bowel syndrome. Gastroenterology. 1995;109(1):40-52.
18. Lembo T, Munakata J, Mertz H, et al. Evidence for the hypersensitivity of lumbar splanchnic afferents in irritable bowel syndrome. Gastroenterology. 1994;107(6):1686-1696.
19. Munakata J, Naliboff B, Harraf F, et al. Repetitive sigmoid stimulation induces rectal hyperalgesia in patients with irritable bowel syndrome. Gastroenterology. 1997;112(1):55-63.
20. Van Ginkel R, Voskuijl WP, Benninga MA, Taminiau JA, Boeckxstaens GE. Alterations in rectal sensitivity and motility in childhood irritable bowel syndrome. Gastroenterology. 2001;120(1):31-38.
21. Verne GN, Robinson ME, Price DD. Hypersensitivity to visceral and cutaneous pain in the irritable bowel syndrome. Pain. 2001;93(1):7-14.
22. Kanazawa M, Hongo M, Fukudo S. Visceral hypersensitivity in irritable bowel syndrome. J Gastroenterol Hepatol. 2011;26(Suppl. 3):119-121.
23. Nozu T, Okumura T. Visceral sensation and irritable bowel syndrome; with special reference to comparison with functional abdominal pain syndrome. J Gastroenterol Hepatol. 2011;26(Suppl. 3):122-127.
24. Manabe N, Wong BS, Camilleri M, Burton D, McKinzie S, Zinsmeister AR. Lower functional gastrointestinal disorders: evidence of abnormal colonic transit in a 287 patient cohort. Neurogastroenterol Motil. 2010;22:293-e82.
25. Sadik R, Bjornsson E, Simren M. The relationship between symptoms, body mass index, gastrointestinal transit and stool frequency in patients with irritable bowel syndrome. Eur J Gastroenterol Hepatol. 2010;22:102-108.
26. Whitehead WE, Burnett CK, Cook 3rd EW, Taub E. Impact of irritable bowel syndrome on quality of life. Dig Dis Sci. 1996;41:2248-2253.
27. Gralnek IM, Hays RD, Kilbourne A, Naliboff B, Mayer EA. The impact of irritable bowel syndrome on health-related quality of life. Gastroenterology. 2000;119:654-660.
28. Pace F, Molteni P, Bollani S, et al. Inflammatory bowel disease versus irritable bowel syndrome: a hospital-based, case-control study of disease impact on quality of life. Scand J Gastroenterol. 2003;38:1031-1038.
29. Sloth H, Jorgensen LS. Chronic non-organic upper abdominal pain: diagnostic safety and prognosis of gastrointestinal and non-intestinal symptoms. A 5- to 7-year follow-up study. Scand J Gastroenterol. 1988;23:1275-1280.
30. Harvey RF, Mauad EC, Brown AM. Prognosis in the irritable bowel syndrome: a 5-year prospective study. Lancet. 1987;1:963-965.
31. Norgaard M, Farkas DK, Pedersen L, et al. Irritable bowel syndrome and risk of colorectal cancer: a Danish nationwide cohort study. Br J Cancer. 2011;104:1202-1206.
32. Mitchell CM, Drossman DA. Survey of the AGA membership relating to patients with functional gastrointestinal disorders. Gastroenterology. 1987;92:1282-1284.
33. Schuster MM. Defining and diagnosing irritable bowel syndrome. Am J Manag Care. 2001;7:S246-S251.
34. Hungin AP, Whorwell PJ, Tack J, Mearin F. The prevalence, patterns and impact of irritable bowel syndrome: an international survey of 40,000 subjects. Aliment Pharmacol Ther. 2003;17:643-650.
35. Talley NJ, Gabriel SE, Harmsen WS, Zinsmeister AR, Evans RW. Medical costs in community subjects with irritable bowel syndrome. Gastroenterology. 1995;109:1736-1741.
36. Jones R, Lydeard S. Irritable bowel syndrome in the general population. BMJ. 1992;304:87-90.
37. Bordie AK. Functional disorders of the colon. J Indian Med Assoc. 1972;58:451-456.
38. O’Keefe EA, Talley NJ, Zinsmeister AR, Jacobsen SJ. Bowel disorders impair functional status and quality of life in the elderly: a population-based study. J Gerontol A Biol Sci Med Sci. 1995;50:M184-M189.
39. Everhart JE, Renault PF. Irritable bowel syndrome in office-based practice in the United States. Gastroenterology. 1991;100:998-1005.
40. Wilson S, Roberts L, Roalfe A, Bridge P, Singh S. Prevalence of irritable bowel syndrome: a community survey. Br J Gen Pract. 2004;54:495-502.
41. Harvey RF, Salih SY, Read AE. Organic and functional disorders in 2000 gastroenterology outpatients. Lancet. 1983;1(8325):632-634.
42. Peery AF, Dellon ES, Lund J, et al. Burden of gastrointestinal disease in the United States: 2012 update. Gastroenterology. 2012;143:1179-1187 e1-3.
43. Sandler RS, Everhart JE, Donowitz M, et al. The burden of selected digestive diseases in the United States. Gastroenterology. 2002;122:1500-1511.
44. Longstreth GF, Thompson WG, Chey WD, Houghton LA, Mearin F, Spiller RC. Functional bowel disorders. Gastroenterology. 2006;130:1480-1491.
45. Guilera M, Balboa A, Mearin F. Bowel habit subtypes and temporal patterns in irritable bowel syndrome: systematic review. Am J Gastroenterol. 2005;100:1174-1184.
46. Mearin F, Balboa A, Badia X, et al. Irritable bowel syndrome subtypes according to bowel habit: revisiting the alternating subtype. Eur J Gastroenterol Hepatol. 2003;15:165-172.
47. Mearin F, Baro E, Roset M, Badia X, Zarate N, Perez I. Clinical patterns over time in irritable bowel syndrome: symptom instability and severity variability. Am J Gastroenterol. 2004;99:113-121.
48. Drossman DA, Morris CB, Hu Y, et al. A prospective assessment of bowel habit in irritable bowel syndrome in women: defining an alternator. Gastroenterology. 2005;128:580-589.
49. Tillisch K, Labus JS, Naliboff BD, et al. Characterization
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