Nutrition and physical activity in inflammatory diseases

Nutrition and Physical Activity

in Infl ammatory Diseases

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Nutrition and Physical Activity

in Infl ammatory Diseases

Edited by

Manohar L. Garg

Nutraceuticals Research Group

University of Newcastle, Australia

and

Lisa G. Wood

Centre for Asthma & Respiratory Diseases

School of Biomedical Sciences & Pharmacy

University of Newcastle, Australia

CABI is a trading name of CAB International

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© CAB International 2013. All rights reserved. No part of this publication

may be reproduced in any form or by any means, electronically,

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permission of the copyright owners.

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

London, UK.

Library of Congress Cataloging-in-Publication Data

Nutrition & physical activity in inflammatory diseases/[edited by] Manohar

L. Garg and Lisa G. Wood.

p. ; cm.

Nutrition and physical activity in inflammatory diseases

Includes bibliographical references and index.

ISBN 978-1-84593-910-6 (alk. paper)

I. Garg, Manohar L. II. Wood, Lisa G. III. C.A.B. International. IV. Title:

Nutrition and physical activity in inflammatory diseases.

[DNLM: 1. Inflammation--physiopathology. 2. Nutritional Physiological

Phenomena. 3. Physical Exertion--physiology. 4. Stress, Physiological. QZ 150]

616’.0473--dc23

2012021014

ISBN-13: 978 1 84593 910 6

Commissioning editor: Rachel Cutts

Editorial assistant: Alexandra Lainsbury

Production editor: Shankari Wilford

Typeset by SPi, Pondicherry, India.

Printed and bound in the UK by the MPG Books Group.

Contents

Preface vii

M.L. Garg and L.G. Wood

Contributors ix

PART 1: INTRODUCTION

1 Inflammation: An Introduction 1

P.C. Calder

PART 2: NUTRITION AND INFLAMMATION

2 Dietary Fats and Inflammation 23

P.C. Calder

3 Carbohydrates and Inflammation 46

A.E. Buyken and J. Brand-Miller

4 Alcohol and Inflammation 61

M.D. Bird and E.J. Kovacs

5 Vitamin D and Inflammation 75

T. Barker

6 Vitamin E and Inflammation 87

T. Barker

7 Vitamin C, B-Complex Vitamins and Inflammation 99

A. Oliveira and C. Lopes

8 Phytonutrients and Inflammation 112

D. Heber

9 Trace Elements and Inflammation 128

S. Samman, H.T. O’Connor, K.S. Bell-Anderson and M. Foster

v

PART 3: PHYSICAL ACTIVITY AND INFLAMMATION

10 Resistance Exercise and Inflammation 145

G. Paulsen and J.M. Peake

11 Endurance Exercise and Inflammation 167

J.M. Peake and J.S. Coombes

PART 4: APPLICATIONS TO DISEASES AND CONDITIONS

12 Obesity and Inflammation 193

M. Bulló and M. Garcia-Aloy

13 Type 2 Diabetes and Inflammation 217

J. Lieffers, B. Hawkins, A. Hofstra, D. Cheung, L.L. McCargar and C.J. Field

14 Cardiovascular Disease and Inflammation 243

A. Heather and K. McGrath

15 Stress and Inflammation: An Emerging Story 260

F.R. Walker, E. Nalivaiko and T.A. Day

16 Depressive Disorders and Inflammation 273

R.K. McNamara

17 Asthma and Inflammation 299

H.A. Scott, M.L. Garg, P.G. Gibson and L.G. Wood

18 Inflammatory Bowel Disease and Inflammation 322

L.R. Ferguson

19 Ageing and Inflammation 338

C. Nowson, J.A. Grieger and D. Cameron-Smith

20 Bone Health and Inflammation 357

M.C. Kruger

21 Eye Health and Inflammation 376

I. Jalbert, B. Golebiowski, F.J. Stapleton and M.C. Madigan

Index 391

vi Contents

vii

Preface

This book presents recent developments and discoveries in the vital areas of inflammation and

related chronic diseases to stimulate further research and to translate such discoveries rapidly

to the interested parties. The information presented in this book includes: an introduction to

inflammation, with special reference to aspects that can be modified by nutrition and physical

activity interventions; a description of how various nutrients affect inflammatory process; a

summary of the impact of aerobic and strength training on inflammatory mediators; and a

comprehensive review of how nutrition and physical activity interventions can be used to

modulate inflammation to prevent the development and progression of chronic diseases

including obesity, diabetes mellitus, cardiovascular disease, eye disease, inflammatory bowel

disease, asthma and arthritis.

Inflammatory mediators originating in a single organ can spill over into the circulation and

influence functioning of other organs. As a result, chronic inflammatory diseases often cluster

together in individuals and are likely to be linked together via the common element, inflam￾mation. Literature describing nutrition and physical activity as modifiers of inflammation

highlights the potential for behavioural interventions to modify a broad range of diseases

using non-pharmacological approaches. This presents an opportunity for multidisciplinary

approaches to be used to tackle the multi-organ perspectives of inflammatory diseases,

involving clinicians, nutritionists, food scientists and exercise physiologists.

Our experience with our own research has been that interventions targeting a specific disease

process are relevant for a variety of other indications. The intention of the book is to compile

knowledge and recent developments that demonstrate the multi-organ effects of chronic

inflammation and the nutritional and physical activity approaches that can be used to reduce

inflammation, particularly when pharmacological approaches alone have struggled to deliver

safe and efficacious disease management.

Manohar L. Garg

Lisa G. Wood

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Contributors

ix

Tyler Barker, The Orthopedic Specialty Hospital, Murray, Utah, USA. E-mail: tyler.barker@

imail.org

Kim Bell-Anderson, Discipline of Nutrition & Metabolism, School of Molecular Bioscience,

University of Sydney, Sydney, New South Wales, Australia.

Jenney Brand-Miller, School of Molecular Bioscience, Boden Institute of Obesity, Nutrition

and Exercise, University of Sydney, Sydney, New South Wales, Australia. E-mail:

[email protected]

Mònica Bulló, Human Nutrition Unit, Faculty of Medicine & Health Sciences, University

Rovira i Virgili, Reus, Tarragona, Spain. E-mail: [email protected]

Anette E. Buyken, Research Institute of Child Nutrition, Rheinische Friedrich-Wilhelms￾Universität Bonn, Dortmund, Germany. E-mail: [email protected]

Philip C. Calder, Human Development and Health Academic Unit, Faculty of Medicine,

University of Southampton, Southampton General Hospital, Southampton, UK. E-mail:

[email protected]

David Cameron-Smith, Centre for Physical Activity and Nutrition Research, School of Exercise

and Nutrition Sciences, Deakin University, Burwood, Victoria, Australia and Liggins

Institute, University of Auckland, New Zealand.

David Cheung, Department of Agricultural, Food & Nutritional Science, Alberta Diabetes

Institute, University of Alberta, Faculty of Medicine & Dentistry, Edmonton, Alberta,

Canada.

Jeff Coombes, School of Human Movement Studies, University of Queensland, Brisbane,

Queensland, Australia. E-mail: [email protected]

Trevor Day, School of Biomedical Sciences & Pharmacy, University of Newcastle, Newcastle,

New South Wales, Australia. E-mail: [email protected]

Lynnette Ferguson, Department of Nutrition, School of Medical Sciences, University of

Auckland, Auckland, New Zealand. E-mail: [email protected]

Catherine Field, Department of Agricultural, Food & Nutritional Science, Alberta Diabetes

Institute, University of Alberta, Faculty of Medicine & Dentistry, Edmonton, Alberta, Canada.

E-mail: [email protected]

Meika Foster, Discipline of Nutrition & Metabolism, School of Molecular Bioscience, University

of Sydney, Sydney, New South Wales, Australia.

Mar Garcia-Aloy, Human Nutrition Unit, Faculty of Medicine & Health Sciences, University

Rovira i Virgili, Reus, Tarragona, Spain.

Manohar Garg, School of Biomedical Sciences & Pharmacy, University of Newcastle, Newcastle,

New South Wales, Australia. E-mail: [email protected]

Peter Gibson, School of Medicine & Public Health, University of Newcastle, Newcastle, New

South Wales, Australia. E-mail: [email protected]

Blanka Golebiowski, School of Optometry and Vision Science, University of New South

Wales, Sydney, New South Wales, Australia.

Jessica A. Grieger, Nutrition and Dietetics, Flinders University, Bedford Park, South Australia,

Australia.

Brianna Hawkins, Department of Agricultural, Food & Nutritional Science, Alberta Diabetes

Institute, University of Alberta, Faculty of Medicine & Dentistry, Edmonton, Alberta, Canada.

Alison Heather, School of Medical and Molecular Biosciences, University of Technology,

Sydney, New South Wales, Australia. E-mail: [email protected]

David Heber, UCLA Center for Human Nutrition, David Geffen School of Medicine, Los

Angeles, California, USA. E-mail: [email protected]

Angela Hofstra, Department of Agricultural, Food & Nutritional Science, Alberta Diabetes

Institute, University of Alberta, Faculty of Medicine & Dentistry, Edmonton, Alberta, Canada.

Isabelle Jalbert, School of Optometry and Vision Science, University of New South Wales,

Sydney, New South Wales, Australia.

Elizabeth J. Kovacs, Department of Surgery, Burn & Shock Trauma Institute, Alcohol Research

Program, Loyola University Medical Centre, Maywood, Illinois, USA. E-mail: [email protected]

Marlena Kruger, Institute of Food, Nutrition & Human Health, Riddett Institute, Massey

University, Palmerston North, New Zealand. E-mail: [email protected]

Jessica Lieffers, Department of Agricultural, Food & Nutritional Science, Alberta Diabetes

Institute, University of Alberta, Faculty of Medicine & Dentistry, Edmonton, Alberta, Canada.

Carla Lopes, Department of Clinical Epidemiology, Predictive Medicine and Public Health,

University of Porto Medical School and Public Health Institute, University of Porto,

Porto, Portugal.

Michele Madigan, School of Optometry and Vision Science, University of New South Wales,

Sydney, New South Wales, and Save Sight Institute, Sydney Medical School, University of

Sydney, Australia. E-mail: [email protected]

Linda McCargar, Department of Agricultural, Food & Nutritional Science, Alberta Diabetes

Institute, University of Alberta, Faculty of Medicine & Dentistry, Edmonton, Alberta, Canada.

Kristine McGrath, School of Medical and Molecular Biosciences, University of Technology,

Sydney, New South Wales, Australia.

Robert K. McNamara, Department of Psychiatry, University of Cincinnati, College of Medicine,

Cincinnati, Ohio, USA. E-mail: [email protected]

Eugene Nalivaiko, School of Biomedical Sciences & Pharmacy, University of Newcastle,

Newcastle, New South Wales, Australia. E-mail: [email protected]

Caryl Nowson, Centre for Physical Activity and Nutrition Research, School of Exercise and

Nutrition Sciences, Deakin University, Burwood, Victoria, Australia. E-mail: nowson@

deakin.edu.au

Helen O’Connor, Discipline of Exercise & Sport Science, Faculty of Health Sciences,

University of Sydney, Sydney, New South Wales, Australia.

Andreia Oliveira, Department of Clinical Epidemiology, Predictive Medicine and Public

Health, University of Porto Medical School and Public Health Institute, University of

Porto, Porto, Portugal. E-mail: [email protected]

Goran Paulsen, Norwegian School of Sports Science, Oslo, Norway. E-mail: Goran.Paulsen@

nih.no

Jonathan Peake, School of Human Movement Studies, University of Queensland, Centre for

Military and Veterans’ Health, University of Queensland, and Centre of Excellence for

Applied Sport Science Research, Queensland Academy of Sport, Brisbane, Queensland,

Australia. E-mail: [email protected]

x Contributors

Contributors xi

Samir Samman, Discipline of Nutrition & Metabolism, School of Molecular Bioscience,

University of Sydney, Sydney, New South Wales, Australia. E-mail: samir.samman@sydney.

edu.au

Hayley Scott, School of Medicine & Public Health, University of Newcastle, Newcastle, New

South Wales, Australia. E-mail: [email protected]

Fiona Stapleton, School of Optometry and Vision Science, University of New South Wales,

Sydney, New South Wales, Australia.

F. Rohan Walker, School of Biomedical Sciences & Pharmacy, University of Newcastle,

Newcastle, New South Wales, Australia. E-mail: [email protected]

Lisa Wood, School of Biomedical Sciences & Pharmacy, University of Newcastle, Newcastle,

New South Wales, Australia. E-mail: [email protected]

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©CAB International 2013. Nutrition and Physical Activity in Inflammatory Diseases

(eds M.L. Garg and L.G. Wood) 1

Introduction 1

Acute and Chronic Inflammation 2

Physiological Role of Principal Cells Involved in Inflammation 4

Neutrophils 4

Eosinophils 5

Basophils 5

Mast cells 6

Mononuclear phagocytes (monocytes and macrophages) 6

Lymphocytes 7

Leucocyte–Endothelium Interactions in Inflammation 7

Characteristics of Chronic Inflammatory Conditions 8

Chronic inflammation of the joints: rheumatoid arthritis (RA) 8

Chronic inflammation of the gastrointestinal mucosa: inflammatory bowel diseases 9

Chronic inflammation of the airways: asthma 9

Chronic inflammation of the skin: psoriasis 10

Chronic inflammation of the vascular wall: atherosclerosis 10

Chronic inflammation of adipose tissue: obesity 11

Common Features of Chronic Inflammatory Conditions and Mediators Involved 11

How to Measure Chronic Inflammation 13

Factors Affecting Inflammation 17

Summary and Conclusions 19

References 20

Inflammation: An Introduction

P.C. Calder*

Human Development and Health Academic Unit,

University of Southampton, Southampton, UK

Introduction

Inflammation is a physiological response to

infection, injury or irritants. It is part of the host’s

defence mechanism, acting to initiate pathogen

killing. Inflammation also plays a role in tissue

repair processes so helping to restore homeo￾stasis at infected or damaged sites. Thus, in its

physiological context, inflammation is protec￾tive. It is considered to be part of the innate

immune system, being initiated by pathogens

and being an essential component of the host

* Author, [email protected]

2 P.C. Calder

response aimed at eliminating pathogens.

Inflammation involves interactions amongst

many cell types and the production of, and

responses to, a number of chemical media￾tors. Without inflammation, pathogens would

not be efficiently eliminated and wounds and

infections would not heal. Chronic inflamma￾tion can, however, damage host tissues and

is a central element in a number of diseases,

such as rheumatoid arthritis, Crohn’s dis￾ease, ulcerative colitis, asthma, dermatitis and

even atherosclerosis and cancer. Because of its

potential to cause damage, it is important that

inflammation is closely regulated.

The five classical signs of inflamma￾tion are pain (dolour), heat (calor), redness

(rubor), swelling (tumour) and loss of func￾tion (functio laesa). The first four signs were

described by Celsus 2000 years ago, whereas

loss of function was recognized and added

later. Redness and heat are due to increased

blood flow to the inflamed site; swelling is

caused by accumulation of fluid at that site;

pain is due to release of chemicals that stim￾ulate nerve endings. Inflammation may be

classified as acute or chronic (Table 1.1).

Acute and Chronic Inflammation

Acute inflammation is the initial response of

the body to harmful stimuli. It is a short-term

process, usually appearing within a few min￾utes or hours and ceasing upon the removal

of the injurious stimulus. Acute inflammation

is initiated by cells already present in tissues

prior to the arrival of the causative agent. These

cells include macrophages, dendritic cells and

mast cells and they express on their surface

receptors known as pattern recognition recep￾tors (PRRs). These recognize molecules that are

general features of pathogens but not the host;

these molecules are termed microbe-associated

molecular patterns (MAMPs). An example

of a PRR is toll-like receptor (TLR) 4 and an

example of a MAMP is the lipopolysaccha￾ride (LPS) structure that is a component of the

cell wall of Gram-negative bacteria (Aderem

and Ulevitch, 2000); LPS is sometimes called

bacterial endotoxin. Upon exposure to an infec￾tious microbe or as the result of another insult

(e.g. a burn, exposure to ultraviolet irradiation

or a penetrating injury) a PRR will recognize

a MAMP and the cell expressing the PRR

becomes activated. As a result, the cell releases

chemicals termed inflammatory mediators. It

is these mediators that are responsible for the

clinical signs of inflammation. Vasodilation

and the increase in blood flow that results

causes the redness and heat. An increased

permeability of blood vessels results in leak￾age of plasma fluid and proteins into the

inflamed site causing a local oedema seen as

swelling. Some of mediators that are released,

e.g. bradykinin, play a role in causing pain,

whereas some cause an increase in permeability

across the blood vessel wall allowing the migra￾tion of leucocytes (these are the white blood

cells) from the bloodstream into the tissue.

These cells are attracted to the site of inflam￾mation as a result of specific mediators, termed

Table 1.1. General features of acute and chronic inflammation.

Acute Chronic

Causative agent Pathogens, injured tissues,

irradiation, irritants

Persistent inflammation owing to

pathogens or other foreign bodies,

autoimmune reactions

Major cells involved Neutrophils and other granulocytes,

mononuclear cells (monocytes,

macrophages)

Mononuclear cells (monocytes,

macrophages, T lymphocytes,

B lymphocytes)

Primary mediators Vasoactive amines, eicosanoids,

granule peptides

Cytokines, eicosanoids, growth

factors, reactive oxygen species,

hydrolytic enzymes

Onset Immediate Delayed

Duration Hours to a few days Up to months or years

Outcomes Resolution, chronic inflammation Tissue destruction, fibrosis, necrosis