SportSNutritioNEditEd by Ronald J. Maughan

tHE ENCYCLopAEDiA oF SportS MEDiCiNEAN ioC MEDiCAL CoMMiSSioN puBLiCAtioN

SPORTS NUTRITION

SPORTS NUTRITION

VOLUME XIX OF THE ENCYCLOPAEDIA OF SPORTS MEDICINE

AN IOC MEDICAL COMMISSION PUBLICATION

EDITED BY

RONALD J. MAUGHAN, PhD

This edition fi rst published 2014 © 2014 International Olympic Committee

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Library of Congress Cataloging-in-Publication DataSports nutrition (John Wiley & Sons)

Sports nutrition/edited by Ronald J. Maughan.

p. ; cm. – (Encyclopaedia of sports medicine ; volume XIX)

“An IOC medical commission publication.”

Includes bibliographical references and index.

ISBN 978-1-118-27576-4 (cloth : alk. paper) – ISBN 978-1-118-69231-8 – ISBN 978-1-118-69232-5 (emobi) –

ISBN 978-1-118-69233-2 (epdf) – ISBN 978-1-118-69235-6

I. Maughan, Ron J., 1951- editor of compilation. II. IOC Medical Commission, issuing body.

III. Title. IV. Series: Encyclopaedia of sports medicine ; v. 19.

[DNLM: 1. Nutritional Physiological Phenomena. 2. Sports–physiology.

3. Athletic Performance. 4. Exercise–physiology. 5. Sports Medicine–methods. QT 13 E527

1988 v.19/QT 260]

RC1235

613.7’11–dc23

2013018143

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

Wiley also publishes its books in a variety of electronic formats. Some content that appears in print may not

be available in electronic books.

Cover image: © IOC/Juilliart

Cover design by Rob Sawkins for Opta Design Ltd

Set in 9/12pt Palatino by Aptara Inc., New Delhi, India

1 2014

v

Contents

List of Contributors, viii

Foreword, xii

Preface, xiii

Part 1 The Underpinning Science

1 Human Nutrition, 3

david a. bender

2 Exercise Physiology, 20

w. larry kenney, robert murray

3 Biochemistry of Exercise, 36

michael gleeson

Part 2 Energy and Macronutrients

4 How to Assess the Energy Costs of Exercise

and Sport, 61

barbara e. ainsworth

5 Energy Balance and Energy Availability, 72

anne b. loucks

6 Assessing Body Composition, 88

timothy r. ackland,

arthur d. stewart

7 Carbohydrate Needs of Athletes in

Training, 102

louise m. burke

8 The Regulation and Synthesis of Muscle

Glycogen by Means of Nutrient Intervention, 113

john l. ivy

9 Carbohydrate Ingestion During Exercise, 126

asker jeukendrup

10 Defi ning Optimum Protein Intakes

for Athletes, 136

stuart m. phillips

11 Dietary Protein as a Trigger for Metabolic

Adaptation, 147

luc j.c. van loon

12 Fat Metabolism During and After Exercise, 156

bente kiens, jacob jeppesen

13 Metabolic Adaptations to a High-Fat Diet, 166

john a. hawley, wee kian yeo

14 Water and Electrolyte Loss and Replacement

in Training and Competition, 174

ronald j. maughan

15 Performance Effects of Dehydration, 185

eric d.b. goulet

16 Rehydration and Recovery After Exercise, 199

susan m. shirreffs

17 Nutritional Effects on Central Fatigue, 206

bart roelands, romain meeusen

vi contents

30 The Aging Athlete, 369

christine a. rosenbloom

31 The Vegetarian Athlete, 382

jacqueline r. berning

32 The Special Needs Athlete, 392

elizabeth broad

33 Overreaching and Unexplained

Underperformance Syndrome:

Nutritional Interventions, 404

paula robson-ansley,

ricardo costa

34 The Traveling Athlete, 415

susie parker-simmons, kylie andrew

35 Environment and Exercise, 425

samuel n. cheuvront,

brett r. ely, randall l. wilber

36 Food and Nutrition Considerations at Major

Competitions, 439

fiona pelly

Part 5 Health-Related and Clinical Sports

Nutrition

37 Nutrition, Physical Activity, and Health, 455

barry braun, benjamin f. miller

38 Exercise, Nutrition, and Infl ammation, 466

michael j. kraakman, martin

whitham, mark a. febbraio

39 Exercise, Nutrition, and Immune Function, 478

david c. nieman

40 The Diabetic Athlete, 490

gurjit bhogal, nicholas peirce

41 The Overweight Athlete, 503

helen o’connor

42 Eating Disorders in Male and Female

Athletes, 513

monica k. torstveit,

jorunn sundgot-borgen

Part 3 Micronutrients and Dietary Supplements

18 Vitamins, Minerals, and Sport Performance, 217

stella l. volpe, ha nguyen

19 Iron Requirements and Iron Status of

Athletes, 229

giovanni lombardi, giuseppe lippi ,

giuseppe banfi

20 Calcium and Vitamin D, 242

enette larson-meyer

21 Exercise-Induced Oxidative Stress: Are

Supplemental Antioxidants Warranted?, 263

john c. quindry, andreas kavazis,

scott k. powers

22 Dietary Phytochemicals, 277

j. mark davis, benjamin gordon,

e. angela murphy, martin d.

carmichael

23 Risks and Rewards of Dietary Supplement Use

by Athletes, 291

ronald j. maughan

24 Creatine, 301

francis b. stephens, paul l.

greenhaff

25 Caffeine and Exercise Performance, 313

lawrence l. spriet

26 Buffering Agents, 324

craig sale, roger c. harris

27 Alcohol, Exercise, and Sport, 336

ronald j. maughan, susan m.

shirreffs

Part 4 Practical Issues

28 The Female Athlete, 347

susan i . barr

29 The Young Athlete, 359

flavia meyer, brian w. timmons

c o n t e n t s v i i

48 Cycling, 584

peter hespel

49 Gymnastics, 596

dan benardot

50 Swimming, 607

louise m. burke, gregory shaw

51 Winter Sports, 619

nanna l. meyer

52 Team Sports, 629

francis holway

53 Weight-Category Sports, 639

hattie h. wright, ina garthe

Index, 651

43 Importance of Gastrointestinal Function to

Athletic Performance and Health, 526

nancy j. rehrer, john mclaughlin,

lucy k. wasse

44 Hyponatremia of Exercise, 539

timothy d. noakes

Part 6 Sport-Specifi c Nutrition: Practical Issues

45 Strength and Power Events, 551

eric s . rawson, charles e.

brightbill, michael j. stec

46 Sprinting: Optimizing Dietary Intake, 561

gary slater, helen o’connor,

bethanie allanson

47 Distance Running, 572

trent stellingwerff

viii

GURJIT BHOGAL, MBChB, MSc, MRCGP, Queen’s

Medical Centre, Nottingham, UK

BARRY BRAUN, PhD, Department of Kinesiology,

University of Massachusetts, Amherst, MA, USA

CHARLES E. BRIGHTBILL, BS, Department of

Exercise Science, Bloomsburg University, Bloomsburg, PA, USA

ELIZABETH BROAD, PhD, Sports Nutrition,

Australian Institute of Sport, Canberra, ACT, Australia

LOUISE M. BURKE, OAM, PhD, APD, Sports

Nutrition, Australian Institute of Sport, Canberra, ACT, Australia

MARTIN D. CARMICHAEL, PhD, Department of

Physical Education and Exercise Studies, College of Education,

Lander University, Greenwood, SC, USA

SAMUEL N. CHEUVRONT, PhD, RD, Thermal &

Mountain Medicine Division, US Army Research Institute of

Environmental Medicine, Natick, MA, USA

RICARDO COSTA, PhD, RD, RSEN, Department of

Nutrition and Dietetics, Faculty of Medicine Nursing and

Health Sciences, Monash University, Melbourne, VIC, Australia

J. MARK DAVIS, PhD, Psychoneuroimmunology of

Exercise and Nutrition Lab, Division of Applied Physiology,

Department of Exercise Science, University of South Carolina,

Columbia, SC, USA

BRETT R. ELY, MS, Thermal & Mountain Medicine

Division, US Army Research Institute of Environmental

Medicine, Natick, MA, USA

TIMOTHY R. ACKLAND, PhD, School of Sport

Science, Exercise and Health, University of Western Australia,

Crawley, WA, Australia

BARBARA E. AINSWORTH, PhD, MPH, Program

in Exercise and Wellness, School of Nutrition and Health

Promotion, Arizona State University, Phoenix, AZ, USA

BETHANIE ALLANSON, Hons Diet, Faculty of

Computing, Health and Science, Edith Cowan University,

Joondalup, WA, Australia

KYLIE ANDREW, M Diet & Nut, Victorian Institute of

Sport, Albert Park, VIC, Australia

GIUSEPPE BANFI, MD, Laboratory of Experimental

Biochemistry and Molecular Biology, IRCCS Galeazzi

Orthopaedic Institute, Milan, Italy; Department of Biomedical

Sciences for Health, University of Milan, Milan, Italy

SUSAN I. BARR, PhD, Faculty of Land and Food Systems,

University of British Columbia, Vancouver, BC, Canada

DAN BENARDOT, PhD, Department of Nutrition,

Division of Health Professions, Byrdine F. Lewis School of

Nursing and Health Professions, Georgia State University,

Atlanta, GA, USA

DAVID A. BENDER, PhD, Emeritus Professor of

Nutritional Biochemistry, University College London, London, UK

JACQUELINE R. BERNING, PhD, RD, CSSD,

Biology Department, University of Colorado, Colorado

Springs, CO, USA

List of Contributors

l i s t o f c o n t r i b u t o r s i x

MARK A. FEBBRAIO, PhD, Cellular and Molecular

Metabolism Laboratory, Baker IDI Heart and Diabetes

Institute, Melbourne, VIC, Australia; Department of

Biochemistry and Molecular Biology, Monash University,

Melbourne, VIC, Australia

INA GARTHE, PhD, Department of Sports Nutrition,

Olympic Sports Centre, Oslo, Norway

MICHAEL GLEESON, PhD, School of Sport, Exercise

and Health Sciences, Loughborough University, Loughborough,

UK

BENJAMIN GORDON, MS, Psychoneuroimmunology

of Exercise and Nutrition Lab, Division of Applied Physiology,

Department of Exercise Science, University of South Carolina,

Columbia, SC, USA

ERIC D.B. GOULET, PhD, Research Centre on Aging

and Faculty of Physical Education and Sports, University of

Sherbrooke, Sherbrooke, QC, Canada

PAUL L. GREENHAFF, PhD, MRC/Arthritis

Research UK Centre for Musculoskeletal Ageing

Research, School of Biomedical Sciences, University of

Nottingham Medical School, Queen’s Medical Centre,

Nottingham, UK

ROGER C. HARRIS, PhD, Junipa Ltd, Newmarket,

Suffolk, UK

JOHN A. HAWLEY, PhD, Exercise Metabolism Group,

School of Medical Sciences, RMIT University, Bundoora, VIC,

Australia

PETER HESPEL, PhD, Exercise Physiology

Research Group, Department of Kinesiology, Faculty of

Kinesiology and Rehabilitation Sciences, KU Leuven,

Leuven, Belgium

FRANCIS HOLWAY, MSc, Departamento de Medicina

Aplicada a los Deportes, Club Atlético River Plate, Buenos

Aires, Argentina

JOHN L. IVY, PhD, Exercise Physiology and Metabolism

Laboratory, Department of Kinesiology and Health Education,

University of Texas, Austin, TX, USA

JACOB JEPPESEN, PhD, Molecular Physiology Group,

Institute of Nutrition, Exercise and Sports, University of

Copenhagen, Copenhagen, Denmark

ASKER JEUKENDRUP, PhD, Gatorade Sports

Science Institute, Barrington, IL, USA; School of Sport and

Exercise Sciences, University of Birmingham, Edgbaston,

Birmingham, UK

ANDREAS N. KAVAZIS, PhD, Department of

Kinesiology, Mississippi State University, MS, USA

W. LARRY KENNEY, PhD, Noll Laboratory,

Pennsylvania State University, University Park, PA,

USA

BENTE KIENS, Dr Scient, Molecular Physiology Group,

Institute of Nutrition, Exercise and Sports, University of

Copenhagen, Copenhagen, Denmark

MICHAEL J. KRAAKMAN, BPhEd (Hons),

Cellular and Molecular Metabolism Laboratory, Baker IDI

Heart and Diabetes Institute, Melbourne, VIC, Australia;

Department of Biochemistry and Molecular Biology, Monash

University, Melbourne, VIC, Australia

ENETTE LARSON-MEYER, PhD, RD,

Nutrition and Exercise Laboratory, Department of Family

and Consumer Sciences, University of Wyoming, Laramie,

WY, USA

GIUSEPPE LIPPI, PhD, Laboratory of Clinical

Chemistry and Hematology, Department of Pathology and

Laboratory Medicine, University Hospital of Parma,

Parma, Italy

GIOVANNI LOMBARDI, PhD, Laboratory of

Experimental Biochemistry and Molecular Biology, IRCCS

Galeazzi Orthopaedic Institute, Milan, Italy

ANNE B. LOUCKS, PhD, Department of Biological

Sciences, Ohio University, Athens, OH, USA

RONALD J. MAUGHAN, PhD, School of Sport,

Exercise and Health Sciences, Loughborough University,

Loughborough, UK

x list of contributors

NICHOLAS PEIRCE, MD, Queen’s Medical Centre,

Nottingham, UK; National Cricket Performance Centre,

Loughborough University, Loughborough, UK

FIONA PELLY, PhD, APD, School of Health and Sport

Sciences, University of the Sunshine Coast, Maroochydore DC,

QLD, Australia

STUART M. PHILLIPS, PhD, Department of

Kinesiology, Exercise Metabolism Research Group, McMaster

University, Hamilton, ON, Canada

SCOTT K. POWERS, PhD, Department of Applied

Physiology and Kinesiology, University of Florida, Gainesville,

FL, USA

JOHN C. QUINDRY, PhD, Department of Kinesiology,

Auburn University, Auburn, AL, USA

ERIC S. RAWSON, PhD, Department of Exercise

Science, Bloomsburg University, Bloomsburg, PA, USA

NANCY J. REHRER, PhD, School of Physical

Education, University of Otago, Dunedin, New Zealand;

Department of Human Nutrition, University of Otago,

Dunedin, New Zealand

PAULA ROBSON-ANSLEY, PhD, Department of

Sports, Exercise and Rehabilitation, Faculty of Health and

Life Sciences, Northumbria University, Newcastle upon

Tyne, UK

BART ROELANDS, PhD, Department of Human

Physiology and Sports Medicine, Vrije Universiteit Brussel,

Brussels, Belgium; Fund for Scientifi c Research Flanders

(FWO), Brussels, Belgium

CHRISTINE A. ROSENBLOOM, PhD, RD, CSSD,

Division of Nutrition, Byrdine F. Lewis School of Health

Professions, Georgia State University, Atlanta, GA, USA

CRAIG SALE, PhD, Sport, Health and Performance

Enhancement (SHAPE) Research Group, Biomedical Life

and Health Sciences Research Centre, School of Science and

Technology, Nottingham Trent University, Nottingham, UK

GREGORY SHAW, BHSc, Sports Nutrition, Australian

Institute of Sport, Canberra, ACT, Australia

JOHN MCLAUGHLIN, MBChB, PhD,

Gastrointestinal Centre, Institute of Infl ammation and Repair,

Faculty of Medical and Human Sciences, University of

Manchester, Manchester, UK; Manchester Academic Health

Sciences Centre, University of Manchester, Salford Royal

Hospital, Salford, UK

ROMAIN MEEUSEN, PhD, Department of Human

Physiology and Sports Medicine, Vrije Universiteit Brussel,

Brussels, Belgium

FLAVIA MEYER, MD, PhD, Exercise Research

Laboratory (LAPEX), Federal University of Rio Grande do Sul

(UFRGS), Porto Alegre, Brazil

NANNA L. MEYER, PhD, RD, CSSD, University of

Colorado, Colorado Springs, CO, USA; United States Olympic

Committee, Colorado Springs, CO, USA

BENJAMIN F. MILLER, PhD, Department of Health

and Exercise Science, Colorado State University, Fort Collins,

CO, USA

E. ANGELA MURPHY, PhD, Department of

Pathology, Microbiology & Immunology, School of Medicine,

University of South Carolina, Columbia, SC, USA

ROBERT MURRAY, PhD, Sports Science Insights,

LLC, Crystal Lake, IL, USA

HA NGUYEN, BS, Department of Nutrition Sciences,

Drexel University, Philadelphia, PA, USA

DAVID C. NIEMAN, DrPH, Human Performance

Laboratory, Appalachian State University, Kannapolis, NC, USA

TIMOTHY D. NOAKES, MBChB, MD, DSc,

UCT/MRC Research Unit for Exercise Science and Sports

Medicine, Department of Human Biology, University of Cape

Town, Sports Science Institute of South Africa, Newlands,

South Africa

HELEN O’CONNOR, PhD, Faculty of Health

Sciences, University of Sydney, Sydney, NSW, Australia

SUSIE PARKER-SIMMONS, MEd, M Diet & Nut,

United States Olympic Committee, Colorado Springs, CO, USA

l i s t o f c o n t r i b u t o r s x i

SUSAN M. SHIRREFFS, PhD, GlaxoSmithKline,

Brentford, Middlesex, UK; School of Sport, Exercise and Health

Sciences, Loughborough University, Loughborough, UK

GARY SLATER, PhD, Faculty of Science, Health and

Education, University of the Sunshine Coast, Maroochydore

DC, QLD, Australia

LAWRENCE L. SPRIET, PhD, Department of Human

Health & Nutritional Sciences, University of Guelph, Guelph,

ON, Canada

MICHAEL J. STEC, MS, Department of Cell,

Developmental, and Integrative Biology, University of

Alabama at Birmingham, Birmingham, AL, USA

TRENT STELLINGWERFF, PhD, Canadian Sports

Institute—Pacifi c, Pacifi c Institute for Sport Excellence,

Victoria, BC, Canada

FRANCIS B. STEPHENS, PhD, MRC/Arthritis

Research UK Centre for Musculoskeletal Ageing Research,

School of Biomedical Sciences, University of Nottingham

Medical School, Queen’s Medical Centre, Nottingham, UK

ARTHUR D. STEWART, BSc, BPE, MPhil, PhD,

Centre for Obesity Research and Epidemiology, Robert Gordon

University, Aberdeen, Scotland, UK

JORUNN SUNDGOT-BORGEN, PhD,

Department of Sport Medicine, Norwegian School of Sport

Sciences, Oslo, Norway

BRIAN W. TIMMONS, PhD, Child Health and

Exercise Medicine Program, McMaster University, Hamilton,

ON, Canada

MONICA K. TORSTVEIT, PhD, Faculty of Health

and Sport Sciences, University of Agder, Kristiansand, Norway

LUC J.C. VAN LOON, PhD, Department of Human

Movement Sciences, NUTRIM School for Nutrition,

Toxicology and Metabolism, Maastricht University Medical

Centre, Maastricht, The Netherlands

STELLA L. VOLPE, PhD, RD, LDN, Department of

Nutrition Sciences, Drexel University, Philadelphia, PA, USA

LUCY K. WASSE, PhD, Gastrointestinal Centre,

Institute of Infl ammation and Repair, Faculty of Medical and

Human Sciences, University of Manchester, Manchester, UK;

Manchester Academic Health Sciences Centre, University of

Manchester, Salford Royal Hospital, Salford, UK

MARTIN WHITHAM, PhD, Cellular and Molecular

Metabolism Laboratory, Baker IDI Heart and Diabetes

Institute, Melbourne, VIC, Australia

RANDALL L. WILBER, PhD, United States Olympic

Committee, Colorado Springs, CO, USA

HATTIE H. WRIGHT, PhD, Centre of Excellence for

Nutrition, Faculty of Health Sciences, North-West University,

Potchefstroom, South Africa

WEE KIAN YEO, PhD, Division of Research and

Innovation, National Sports Institute of Malaysia, Kuala

Lumpur, Malaysia

xii

volume appears in this rapidly expanding fi eld of

research and practice.

A highly qualifi ed team of international author-

ities present a comprehensive coverage of macro-

nutrients, micronutrients, and dietary supplements

for the athlete. Extensive coverage is given both to

general practical issues and to sports-specifi c issues.

Professor Ronald J. Maughan has been a fre-

quent contributor to both the Encyclopaedia of Sports Medicine series and the Handbook of Sports Medicine and Science series as published by the IOC Medical

Commission. We welcome with great appreciation

his latest publication project related to the science

and medicine of sport.

Dr Jacques Rogge

IOC President

The publication of the Encyclopaedia of Sports Medi-cine, Volume VII Nutrition in Sport, by the IOC Medi-

cal Commission in 2000 constituted a milestone in

the rapid growth of research on sports nutrition

during the last quarter century. Concomitant with

this growth has been the increasing body of evi-

dence concerning the important interactive roles of

proper nutrition and a balanced program of physi-

cal exercise for each person’s health and welfare.

Since the appearance of that volume, a large

amount of research has appeared in scientifi c jour-

nals concerning the role of nutrition in the training

programs of athletes and in their preparation for

competition. It is, therefore, timely that this new

Foreword

xiii

Preface

A comparison of the content of the two volumes

will reveal some constants and some changes. Per-

haps the most important change that has taken

place in recent years is the recognition that the pri-

mary role of nutrition in the athlete’s life is to sup-

port consistent training and to enhance the process

of adaptation that takes place in every tissue of the

body in response to each individual training ses-

sion. It is the sum of these vanishingly small incre-

mental changes that translates into an enhanced

performance. Nutrition support is more about

promoting those changes rather than simply allow-

ing the athlete to recover more effectively between

training sessions and, therefore, to train harder.

Training harder undoubtedly brings some benefi ts

in terms of performance improvement, but it also

brings increased risks of illness and injury. Training

more effectively, rather than just training harder, is

surely a better option.

Those who work at the molecular level have

given us an understanding of the signaling path-

ways within cells that modulate gene expression in

response to training and diet. This understanding

was almost completely absent until very recently,

and these new approaches have great promise for

identifying strategies that might allow even bet-

ter performances than those of today’s athletes. At

the same time, however, there has been a renewed

interest in the adaptations that take place at the

whole body level, including perhaps especially the

links between the brain and the peripheral tissues.

The two approaches, the molecular and the whole

body, have emphasized the individuality of the res-

ponse to both diet and exercise and of the need for

Most of us eat every day, indeed several times every

day. What we eat will affect how we feel and how

we perform, both in the short term and in the long

term. The immediate effects are often small and eas-

ily dismissed. However, after only a short period—

a few days at most—without food, performance in

most tests of physical and mental performance will

inevitably decline. Similar effects are seen if some

food is allowed but the intake of carbohydrate or

water is restricted. It is easy, therefore, to demon-

strate the impact of nutrition on athletic perfor-

mance. Nutrition, though, has many far more subtle

effects on the athlete’s well-being and performance.

A whole range of essential nutrients must be sup-

plied in the right amounts and at the right times if

health and performance are to be optimized. Food,

and the pleasures as well as the nutrients it gives to

the consumer, is a vital part of everyday life. Sports

nutrition must therefore be concerned not only with

the identifi cation of the athlete’s nutritional goals but

also with the translation of these goals into an eating

strategy that takes account of personal preferences,

social and cultural issues, and a whole range of other

factors.

The Medical Commission of the International

Olympic Committee (IOC) has consistently recog-

nized the importance of nutrition in every aspect

of the elite athlete’s life. In choosing to commission

a new encyclopedia volume on the relationships

between diet and performance, the IOC has recog-

nized the great changes that have taken place in our

understanding since the publication of the earlier

version that appeared three Olympic cycles previ-

ously.

xiv preface

view of the key issues. Those who seek to advise

athletes or whose aspiration is to make the next

great advance in our understanding must be pre-

pared to dig much deeper, but perhaps this volume

will provide a framework and a reference point for

further study.

Ronald J. Maughan

Loughborough, UK

individualization and periodization of nutrition

strategies to allow athletes to reach their genetic

potential.

The contributors to this book are, without excep-

tion, world leaders in their fi elds. Each has given

unstintingly of their knowledge and experience in

preparing their chapters. The result is a substan-

tial volume, but such is the scope of the science and

practice of sports nutrition that even this can be no

more than an introduction to the fi eld and an over-

PART 1

THE UNDERPINNING

SCIENCE

Sports Nutrition, 1st Edition. Edited by Ronald J. Maughan.

© 2014 International Olympic Committee. Published 2014 by

John Wiley & Sons, Ltd.

3

Chapter 1

Human Nutrition

DAVID A. BENDER

University College London, London, UK

tissue with increasing age (even when body weight

remains constant). The gender difference is because

women have a greater percentage of body weight as

essential and storage adipose tissue than do men.

Table 1.1 shows equations for calculating BMR from

age, gender, body weight, and height.

The energy cost of different activities is most

commonly expressed as a multiple of BMR—the

physical activity ratio (PAR) for any given activity.

As shown in Table 1.2, PAR ranges from about 1.2×

BMR for sedentary activities up to 6× or more times

BMR for vigorous exercise, and signifi cantly higher

for some sports. Table 1.3 shows the classifi cation of

occupational work by PAR over the 8-hour working

day, excluding leisure activities.

Summing the PAR for different activities through-

out the day, multiplied by the time spent in each

activity as a fraction of 24 hours, allows the calcu-

lation of a person’s physical activity level (PAL),

again as a multiple of BMR. A person’s total energy

expenditure is then (PAL × BMR) + an allowance for

diet-induced thermogenesis (DIT)—the energy cost

of digestion and absorption, plus the cost of synthe-

sizing glycogen, fat, and protein after a meal. DIT is

about 10–15% of the energy yield of a meal. For peo-

ple with a markedly sedentary lifestyle BMR may

represent 80–90% of total energy expenditure.

Measurement of BMR and Energy Expenditure

in Activity

The gold standard method of measuring BMR and

energy expenditure in an activity is by measurement

of heat output from the body. This is done using

a calorimeter—an insulated chamber in which a

The fi rst requirement in human nutrition is for an

energy source; the metabolic fuels that provide this

are carbohydrates, fats, protein, and alcohol. There

is also a need for protein, not only in growth when

the total amount of protein in the body is increasing

but also throughout life to permit turnover of tissue

proteins. In addition, there is a need for some essen-

tial fatty acids and for relatively small amounts

(milligrams or micrograms per day) of vitamins and

minerals.

Energy Nutrition

Even when completely at rest there is a requirement

for energy to maintain nerve and muscle tone, cir-

culation and breathing, and metabolic homeosta-

sis. When measured under controlled conditions

of thermal neutrality (so that energy is not being

expended in keeping warm or cooling down) and

completely at rest (but not asleep, since some people

increase their metabolic rate when asleep, while

others reduce it), this is the basal metabolic rate

(BMR). When the measurement is made under less

strictly controlled conditions, the result is termed

the resting metabolic rate (RMR). BMR depends on

body weight, age, and gender and refl ects mainly

the metabolically more active lean tissues of the

body, although adipose tissue makes a modest

contribution to BMR. The effect of age on BMR

refl ects the replacement of muscle tissue by adipose

4 chapter 1

Table 1.1 Equations for estimating basal metabolic rate from weight or weight and height, at different ages

Age (years)

Males Females

MJ/day kcal/day MJ/day kcal/day

0–3 0.2548w − 0.226 60.9w − 54 0.255w − 0.213 61.0w − 51

0.007w + 6.349h − 2.584 1.673w + 1517h − 617 0.068w + 4.281h − 1.730 16.252w + 1023h − 413

3–10 0.0949w + 2.07 22.7w + 495 0.0941w + 2.09 22.5w + 499

0.082w + 0.545h + 1.736 19.59w + 130h + 415 0.071w + 0.677h + 1.5453 16.97w + 161h + 531

10–17 0.0732w + 2.72 17.5w + 651 0.0510w + 3.12 12.2w + 746

0.068w + 0.574h + 2.157 16.25w + 137h + 516 0.035w + 1.948h + 0.837 8.365w + 465h + 200

18–29 0.0640w + 2.84 15.3w + 679 0.0615w + 2.08 14.7w + 496

0.063w − 0.042h + 2.953 15.06w + 10.04h + 705 0.057w + 1.184h + 0.411 13.62w + 283h + 98

30–59 0.0485w + 3.67 11.6w + 879 0.0364w + 3.47 8.7w + 829

0.048w − 0.011h + 3.670 11.47w + 2.629h + 877 0.034w + 0.006h + 3.530 8.126w + 4.434h + 843

>60 0.0565w + 2.04 13.5w + 487 0.0439w + 2.49 10.5w + 596

Source: Data reported by Schofi eld (1985a, 1985b); recalculated for estimation of BMR in kcal. w, body weight (kg); h, height (m).

Table 1.2 Energy cost of activity, by Physical Activity Ratio (PAR) or multiple of BMR

PAR

1.0–1.4 Lying, standing, or sitting at rest, e.g., watching TV, reading, writing, eating, playing cards, and

board games

1.5–1.8 Sitting: sewing, knitting, playing piano, drivingStanding: preparing vegetables, washing dishes, ironing, general offi ce and laboratory work

1.9–2.4 Standing: mixed household chores, cooking, playing snooker or bowls

2.5–3.3 Standing: dressing, undressing, showering, making beds, vacuum cleaningWalking: 3–4 km/h, playing cricketOccupational: tailoring, shoemaking, electrical and machine tool industry, painting and

decorating

3.4–4.4 Standing: mopping fl oors, gardening, cleaning windows, table tennis, sailingWalking: 4–6 km/h, playing golfOccupational: motor vehicle repairs, carpentry and joinery, chemical industry, bricklaying

4.5–5.9 Standing: polishing furniture, chopping wood, heavy gardening, volley ballWalking: 6–7 km/hExercise: dancing, moderate swimming, gentle cycling, slow joggingOccupational: laboring, hoeing, road construction, digging and shoveling, felling trees

6.0–7.9 Walking: uphill with load or cross-country, climbing stairsExercise: jogging, cycling, energetic swimming, skiing, tennis, football

Source: Department of Health (1991) and WHO (1985).

h u m a n n u t r i t i o n 5

confi ned to the laboratory. If the production of car-

bon dioxide is also measured then it is possible to

calculate the relative amounts of fat, carbohydrate,

and protein being metabolized from the respiratory

quotient (RQ)—the ratio of carbon dioxide pro-

duced to oxygen consumed. When carbohydrate is

being oxidized the RQ = 1, while for fat oxidation

RQ = 0.707. The amount of protein being metabo-

lized can be calculated separately from the excretion

of urea, the end product of amino acid metabolism.

If respirometry includes the measurement of car-

bon dioxide and oxygen, as well as urinary nitrogen,

then it is possible to estimate both energy expendi-

ture and the proportions of different fuels being uti-

lized, from the following formulae (Weir, 1949):

• Energy expenditure (kJ) = 16.849 × ml oxygen con-

sumed + 4.628 × ml carbon dioxide produced  −

9.079 × g N excreted

• Energy expenditure (kcal) = 4.025 × ml oxygen

consumed + 1.106 × ml carbon dioxide pro-

duced − 2.168 × g N excreted

If urinary nitrogen is not determined, and it is

assumed that protein provides 15% of energy, then

• Energy expenditure (kJ) = 16.318 × ml oxygen

consumed + 4.602 × ml carbon dioxide produced

• Energy expenditure (kcal) = 3.898 × ml oxygen

consumed + 1.099 × ml carbon dioxide produced

The amount of each fuel being utilized can be cal-

culated from

• Grams carbohydrate oxidized = 4.706 × ml carbon

dioxide produced − 3.340 × ml oxygen con-

sumed − 2.714 × g N excreted

constant temperature is maintained by running cold

water through pipes and measuring the increase in

the temperature of the water. Obviously, the range

of activities that can be achieved in a small chamber

is limited, and rather than direct calorimetry, most

studies use indirect calorimetry, i.e., the measure-

ment of the rate of oxygen consumption (Levine,

2005). As shown in Table 1.4, to fi rst approximation,

1 liter of oxygen consumed is equivalent to 20 kJ of

energy expenditure. This means that measurement

of oxygen consumption can be used to estimate

energy expenditure in a wide range of activities, not

Table 1.3 Classifi cation of types of occupational work

by PAR (average PAR through 8-hour working day,

excluding leisure activities)

PAR

Men Women

Light 1.7 1.7 Professional, clerical,

and technical workers,

administrative and

managerial staff, sales

representatives, housewives

Moderate 2.7 2.2 Sales staff, domestic service,

students, transport workers,

joiners, roofi ng workers

Moderately

heavy

3.0 2.3 Machine operators,

laborers, agricultural

workers, forestry, hunting

and fi shing, bricklaying,

masonry

Heavy 3.8 2.8 Laborers, agricultural

workers, bricklaying,

masonry where there is

little or no mechanization

Source: Department of Health (1991).

Table 1.4 Oxygen consumption and carbon dioxide production in the oxidation of metabolic fuels

Energy

yield (kJ/g)

Oxygen

consumed (l/g)

Carbon dioxide

produced (l/g)

Respiratory

quotient (CO2/O2)

Energy/oxygen

consumption (kJ/l oxygen)

Carbohydrate 16 0.829 0.829 1.0 19.3

Protein 17 0.966 0.782 0.809 17.5

Fat 37 2.016 1.427 0.707 18.35

6 chapter 1

From records of food eaten, the average RQ over the

period can be estimated and hence, allowing for any

changes in body weight, the total oxygen consump-

tion and energy expenditure can be calculated.

Recommendations and Reference Levels for

Energy Intake

Unlike reference intakes for protein and micronu-

trients which allow a margin of 2× standard devia-

tion above the observed average requirement, so as

to allow for individual variation and cover almost

all of the population, reference levels for energy

intake (see Table 1.5) are based on average require-

ments, since adding 2× standard deviation would

result in half the population being over-provided

with energy, and hence contribute to the devel-

opment of obesity. At its simplest, energy intake

should match energy expenditure and hence,

assuming that body weight is within the desirable

range (a body mass index of 20–25 kg/m2), should

be such that a constant body weight is achieved.

• Grams fat oxidized = 1.768 × ml oxygen con-

sumed  − 1.778 × ml carbon dioxide produced −

2.021 × g N excreted

• Grams protein oxidized = 6.25 × g N excreted

Although classical respirometer studies have

allowed the measurement of energy expenditure in

many activities (and indeed provided the data for

PAR shown in Table 1.2), such studies are, of neces-

sity, short term. A more recent development has

been the use of double stable isotopically labeled

water (2H218O), which provides a noninvasive

method of measuring energy expenditure over a

period of 1–3 weeks. As shown in Figure 1.1, the

label from 18O is lost from the body faster than that

from 2H. This is because the labeled hydrogen is lost

from the body only as water, while the oxygen is

lost in both water and carbon dioxide, because of

the rapid equilibrium between carbon dioxide and

bicarbonate (Heymsfi eld et al., 2006; Ritz & Cow-

ard, 1995; Speakman, 1997).

Following an oral dose of 2H218O, the iso-

topic enrichment of water in plasma, saliva, or

urine is determined at intervals over a period of

10–21 days. The rate of carbon dioxide production

is then calculated from the greater rate of loss of 18O than 2H, as

• Carbon dioxide production rate = (0.5 × total

body water) × (rate constant for 18O disappear-

ance − rate constant for 2H disappearance)

0

Rela

tive isoto

pe e

nrichm

ent

0

20

40

60

80

100

5 10 15 20 25

Time (days)

2H

18O

Figure 1.1 Loss of label from 2H218O—the basis of the

dual isotopically labeled water method for estimating

total energy expenditure.

Table 1.5 Estimated average requirements for energy

Males Females

Age MJ/day kcal/day MJ/day kcal/day

0–3 months 2.28 545 2.06 515

4–6 months 2.89 690 2.69 645

7–9 months 3.44 825 3.20 765

10–12 months 3.85 920 3.61 865

1–3 years 5.15 1230 4.86 1165

4–6 years 7.16 1715 6.46 1545

7–10 years 8.24 1970 7.28 1740

11–14 years 9.27 2220 7.92 1845

15–18 years 11.51 2755 8.83 2110

19–50 years 10.6 2550 8.10 1940

51–59 years 10.6 2550 8.00 1900

60–64 years 9.93 2380 7.99 1900

65–74 years 9.71 2330 7.96 1900

>75 years 8.77 2100 7.61 1810

Source: Department of Health (1991).

h u m a n n u t r i t i o n 7

a contributory factor in atherosclerosis and cor-

onary artery disease. The current consensus is

that fat should provide 30% of energy intake for

the general population (Prentice, 2005), though

the fraction may be higher or lower for athletes,

depending on the training load and therefore

on the energy demand. At very low fat intakes,

it is diffi cult to absorb the fat-soluble vitamins

A, D, E, and K, which are absorbed in lipid

micelles together with the products of dietary fat

digestion.

The type of dietary fat is also important.

Figure  1.2 shows the families of fatty acids and

Table 1.6, the main dietary fatty acids. There is

a convenient shorthand notation for fatty acids

showing the number of carbon atoms, and the

number of double bonds and the position of the

fi rst double bond from the methyl group as either

n–3, 6, or 9 or ω3, 6, or 9.

Carbohydrate, Fat, and Protein as Metabolic Fuels

There is no absolute requirement for a dietary

source of carbohydrate or fat (apart from essential

fatty acids, see below), but there is a need to main-

tain an adequate supply of glucose for the brain

(which is largely dependent on glucose) and red

blood cells (which are completely dependent on

glucose).

The current consensus (Prentice, 2005) is that

carbohydrates should provide about 55% of

energy intake for the general population, largely

as starches and other complex carbohydrates,

with sugars providing no more than about 10% of

energy intake. For athletes, it is more common to

express daily carbohydrate requirements in abso-

lute terms, as grams of carbohydrate per kilogram

of body mass, as this is independent of energy

intake which may vary widely. Sugars are divided

into intrinsic sugars, contained within the cells of

plant foods, and extrinsic sugars in free solution;

it is these extrinsic sugars that should be limited,

mainly to reduce the risk of dental caries and also

because it is easy to overconsume sugars in bever-

ages, etc., leading to obesity. In the United King-

dom, lactose in milk is considered separately from

other extrinsic sugars, since it does not contribute

to the development of dental caries and milk is

an important source of calcium and ribofl avin in

most diets.

Glucose needs for the brain and red blood cells

can be met by gluconeogenesis from amino acids

and glycerol in fasting (or when the diet is low in

carbohydrate and high in protein), albeit at a rela-

tively high energy cost. The increase in metabolic

rate associated with gluconeogenesis explains much

of the weight loss associated with very low carbohy-

drate diets that permit more or less unlimited con-

sumption of protein-rich foods.

When the diet provides less than about 15% of

energy from fat, it is diffi cult to eat a suffi cient

volume of food to meet energy requirements.

Conversely, when the diet provides more than

about 35% of energy from fat it is easy to overcon-

sume food, leading to obesity. More importantly,

a high fat intake leads to persistence of athero-

genic chylomicron remnants in the bloodstream,

OH

OH

O

OH

O

Saturated fatty acid (stearic acid, C18:0)

Monounsaturated fatty acid (oleic acid, C18: ω19)

Polyunsaturated fatty acid (linoleic acid, C18:2 ω6)

Polyunsaturated fatty acid (α-linolenic acid, C18:3 ω3)OH

O

cis-

trans-

Figure 1.2 The families of fatty acids and cis–trans isom-

erism in unsaturated fatty acids.

8 chapter 1

fatty acids are poor substrates for esterifi cation of

cholesterol, while monounsaturated are better, and

polyunsaturated are the best substrates. Stearic acid

(C18:0), although saturated, has less adverse effect

on LDL cholesterol than other saturated fatty acids

because it is readily unsaturated to oleic acid (C18:1

ω9). It is recommended that no more than one-third

of fat intake (10% of energy intake) should be from

saturated fatty acids, with 6% from polyunsaturated

fatty acids.

Trans-isomers of unsaturated fatty acids arise

during the catalytic hydrogenation of vegetable

oils to yield spreadable fats, and also occur in mod-

est amounts in fats from ruminants. They do not

have the same benefi cial effect on LDL cholesterol

as do the cis-isomers, but are atherogenic, and may

adversely affect the fl uidity of cell membranes. It

is therefore recommended that trans-fatty acids

should provide less than 2% of energy intake (Brit-

ish Nutrition Foundation, 1995).

As shown in Figure 1.2, there are three families

of unsaturated fatty acids, with the fi rst double

bond at the ω3, ω6, or ω9 position. Human beings

have an enzyme that can introduce a double bond

into a saturated fatty acid at the ω9 position and

enzymes that can introduce double bonds between

ω3 or ω6 and the carboxyl group, but not between

ω9 and the methyl group. This means that there is

a requirement for a dietary source of both ω3 and

ω6 polyunsaturated fatty acids, which are precur-

sors of prostaglandins and other eicosanoids that

acts as signaling molecules. These are the essential

fatty acids—linoleic and linolenic acids, which can

undergo chain elongation and further desaturation

in the body. The same enzymes are involved in the

chain elongation, desaturation, and onward metab-

olism to eicosanoids for both ω3 and ω6 polyunsatu-

rated fatty acids, and the balance between the two

families of fatty acids in the diet, is important.

In addition to the requirement for protein per se,

protein must also be considered as a metabolic fuel.

For an adult in nitrogen balance, whose total body

protein content is constant, an amount of amino

acids equivalent to the dietary intake of protein

will be metabolized each day, as an energy source.

The metabolism of amino acids is less effi cient than

that of carbohydrates, since there are a number of

High intakes of saturated fatty acids lead to an

increase in low-density lipoprotein (LDL) chol-

esterol and are therefore a major factor in atherogen-

esis. Compared with monounsaturated fatty acids,

saturated fatty acids lead to an increase in LDL

cholesterol proportional to twice the intake. Polyun-

saturated fatty acids lead to a decrease in LDL chol-

esterol proportional to their intake (Anderson et al.,

1957; Armstrong et al., 1957; Hegsted et al., 1965,

1993; Keys et al., 1957). This is because saturated

Table 1.6 Fatty acid nomenclature

C atoms

Double bonds

ShorthandNumber First

Saturated

Butyric 4 0 – C4:0

Caproic 6 0 – C6:0

Caprylic 8 0 – C8:0

Capric 10 0 – C10:0

Lauric 12 0 – C12:0

Myristic 14 0 – C14:0

Palmitic 16 0 – C16:0

Stearic 18 0 – C18:0

Arachidic 20 0 – C20:0

Behenic 22 0 – C22:0

Lignoceric 24 0 – C24:0

Monounsaturated

Palmitoleic 16 1 7 C16:1 ω7

Oleic 18 1 9 C18:1 ω9

Nervonic 24 1 9 C24:1 ω9

Polyunsaturated

Linoleic 18 2 6 C18:2 ω6

α-Linolenic 18 3 3 C18:3 ω3

γ-Linolenic 18 3 6 C18:3 ω6

Arachidonic 20 4 6 C20:4 ω6

Eicosapentaenoic 20 5 3 C20:5 ω3

Docosatetraenoic 22 4 6 C22:4 ω6

Docosapentaenoic 22 5 3 C22:5 ω3

Docosapentaenoic 22 5 6 C22:5 ω6

Docosahexaenoic 22 6 3 C22:6 ω3

h u m a n n u t r i t i o n 9

a safe level of protein intake is set at 0.8 g/kg body

weight or 56  g/day for a 70  kg adult. Safe here

means safe and (more than) adequate to prevent

defi ciency and does not imply that higher levels

of intake are unsafe, although there is some evi-

dence that exceptionally high levels of habitual

protein intake are associated with bone and kid-

ney disease.

The safe level of protein intake is equivalent

to 8–9% of energy from protein, so that people in

western countries consuming the recommended

14–15% of energy from protein are more than ade-

quately supplied. However, the 10% increase in the

estimated average requirement of the 2007 report

greatly increases the number of people in develop-

ing countries whose protein intake is deemed mar-

ginal or inadequate.

Protein Quality and Amino Acid Requirements

The need for protein is not just for total protein, but

for an intake of amino acids in the amounts required

for body protein synthesis and turnover. Classical

studies of the amounts of individual amino acids

required to maintain N balance in the 1950s and

1960s established that 8 of the 20 amino acids found

in body proteins are dietary essentials and cannot

be synthesized in the body. These essential or indis-

pensable amino acids are isoleucine, leucine, lysine,

methionine, phenylalanine, threonine, tryptophan,

and valine. It was not until 1975 that histidine was

also recognized to be an essential amino acid; for

reasons that are unclear, it is possible to maintain N

balance on a histidine-free diet for at least a week.

These early studies permitted determination of the

amounts of each essential amino acid needed to

maintain N balance, as shown in Table 1.7.

More recent studies have attempted to deter-

mine the requirements for essential amino acids

using amino acids labeled with the stable iso-

topes 15N or 13C. One approach is to measure the

incorporation of the labeled amino acid of interest

into body proteins, and its subsequent catabolism

and the excretion of 13CO2 or 15N urea. The prob-

lem with this direct approach is that the amount

of stable isotopically labeled amino acid that has

to be administered in order to achieve adequate

thermogenic steps in which ATP is synthesized and

then consumed (Bender, 2012) but, nevertheless,

protein can be a factor in the development of obesity

if total energy intake is greater than expenditure. If

carbohydrate is to provide 55% of energy and fat

30%, the recommendation is that protein should

provide 14–15% of energy (with alcohol, if con-

sumed, providing about 1%). This is almost twice

the requirement for protein turnover. Athletes with

a high energy intake can achieve an adequate pro-

tein intake even if protein accounts for even a much

lower fraction of total energy intake.

Protein Requirements

For an adult whose total body protein content is

constant, the intake of nitrogenous compounds

(mainly protein) in the diet will be equal to the uri-

nary and fecal losses of nitrogenous compounds.

This is nitrogen (N) balance or equilibrium. If the

dietary protein intake is inadequate then the losses

of N will be greater than the intake—negative N bal-

ance and a net loss of body protein. This also occurs

in response to a variety of pathological conditions.

In growth, pregnancy, and recovery from losses

there will be positive N balance—excretion is less

than intake and there is an increase in total body

protein.

The determination of protein requirements

remains controversial. Apart from times of growth

and recovery from losses, N balance can be main-

tained at any level of protein intake above the

requirement. In principle, it is easy to measure N

balance in people maintained at different levels of

protein intake and so determine their requirement.

The problem is that the rates of protein turnover

and catabolism of amino acids change with protein

intake, so that apparent protein requirements are

infl uenced by prior protein intake. This means that

studies of N balance require a long period of adap-

tation at each level of intake.

Reexamination of the results of N balance stud-

ies led to the 2007 WHO/FAO/UNU report (WHO,

2007) that increased the average requirement for

protein by 10%, from the previously accepted fi g-

ure of 0.6 g of protein/kg body weight/day to 0.66.

Allowing for individual variation in requirements,

10 chapter 1

Table 1.7 Reference patterns of essential amino acids

From N balance studies From stable isotope studies

mg/kg bw/day mg/g protein mg/kg bw/day mg/g protein

Histidine – – 10 15

Isoleucine 10 15 20 30

Leucine 14 21 39 59

Lysine 12 18 30 45

Methionine + cysteine 13 20 15 22

Methionine – – 10 16

Cysteine – – 4 6

Phenylalanine + tyrosine 14 21 25 38

Threonine 7 11 15 23

Tryptophan 3.5 5 4 6

Valine 10 15 26 39

Total essential amino acids 93.5 141 184 277

Source: WHO (2007).

sensitivity is so large that it distorts the body

pool of the amino acid and so overestimates the

apparent requirement.

The alternative approach is the indicator amino

acid method, in which varying amounts of the

amino acid of interest are fed and the catabolism

of a different essential amino acid (the indicator

amino acid) is measured. The principle here is that

when the amino acid of interest has been depleted

then all of the remaining indicator amino acid will

be catabolized, since it cannot be used for further

protein synthesis. Estimates of essential amino acid

requirements by isotope tracer methods are shown

in Table 1.7.

The essential amino acid that is present in diet-

ary protein in the least amount compared with the

requirement for body protein synthesis is termed

the limiting amino acid. Once supplies of this amino

acid have been exhausted, protein synthesis comes

to a halt and the remaining amino acids are catabo-

lized as metabolic fuel.

Two of the amino acids can only be synthesized

in the body from essential precursors: tyrosine

from phenylalanine and cysteine from methionine.

Providing these in the diet thus spares the require-

ment for the parent amino acid. This is especially

important in the case of cysteine and methionine

since, in many diets, it is the sum of these two amino

acids that is limiting.

The remaining amino acids are generally con-

sidered to be nonessential or dispensable, since

they can be synthesized in the body from more or

less common metabolic intermediates. However,

only three amino acids can be considered to be

completely dispensable since they are synthesized

from ubiquitous intermediates of carbohydrate

metabolism: alanine from pyruvate, glutamate from

2-oxoglutarate, and aspartate from oxaloacetate.

The remaining amino acids (arginine, asparagine,

glutamine, glycine, proline, and serine) must all

be considered to be semi-essential, in that under

conditions of metabolic stress or rapid growth the

capacity for their synthesis may be inadequate to

meet requirements.

The nutritional value or quality of individual

proteins depends on whether or not they contain

the essential amino acids in the amounts that are

required. A number of different ways of determin-

ing protein quality have been developed:

• Biological value (BV) is the proportion of

absorbed protein that is retained in the body. A

h u m a n n u t r i t i o n 1 1

quality between the “best” diets in devel-

oped countries and the “worst” in developing

countries.

2. The quality of the dietary protein is only impor-

tant when the total protein intake is marginal. If

the total amount of protein consumed is signifi -

cantly greater than requirements then the quality

of that protein is irrelevant.

Micronutrients: Vitamins and Minerals

Minerals

Any chemical element that has a metabolic or

other function in the body is obviously a dietary

essential, since elements cannot be interconverted.

Table 1.8 shows the minerals that are known to

be dietary essentials, classifi ed by their functions.

Some minerals appear under more than one head-

ing, since they have multiple functions in the body.

There is a small group of minerals (silicon, vana-

dium, nickel, and tin) that are known to be dietary

protein that is completely useable (e.g., egg and

human milk) has a BV of 0.9–1; meat and fi sh

have a BV of 0.75–0.8; wheat protein has a BV of

0.5; gelatin (which completely lacks tryptophan)

has a BV of 0.

• Net protein utilization (NPU) is the proportion of

dietary protein that is retained in the body (i.e., it

takes account of the digestibility of the protein).

By convention, it is measured at 10% dietary pro-

tein, at which level the experimental animal can

utilize all of the protein as long as the balance of

essential amino acids is correct.

• Protein effi ciency ratio (PER) is the gain in weight

of growing animals per gram of protein eaten.

• Relative protein value (RPV) is the ability of a test

protein, fed at various levels of intake, to sup-

port nitrogen balance, compared with a standard

protein.

• Chemical score is based on chemical analysis of

the amino acids present in the protein; it is the

amount of the limiting amino acid compared with

the amount of the same amino acid in egg protein

(which is completely useable for tissue protein

synthesis).

• Protein score (or amino acid score) is again based

on chemical analysis, but uses a reference pattern

of amino acid requirements as the standard. This

provides the basis of the legally required way of

expressing protein quality in the United States—

the protein digestibility-corrected amino acid

score (PDCAAS).

All of these measures of protein quality suffer from

two problems in practical nutrition:

1. No one eats a single food as their only protein

source. While individual vegetable proteins

may have a low BV, cereals are generally limited

by lysine (and hence have a relative excess of

the sulfur amino acids methionine + cysteine),

while legume proteins are limited by the sulfur

amino acids and hence have a relative excess

of lysine. There is complementation between

the amino acids in different proteins in a meal,

and a judicious mixture of cereals and legumes

can have a BV as high as that of meat. World-

wide there is very little difference in protein

Table 1.8 Essential minerals classifi ed by their function

Structural function Calcium, magnesium,

phosphate

Involved in membrane

function

Sodium, potassium

Function as prosthetic

groups in enzymes

Cobalt, copper, iron,

molybdenum, selenium,

zinc

Regulatory role or role in

hormone action

Calcium, chromium,

iodine, magnesium,

manganese, sodium,

potassium

Known to be essential, but

function unknown

Silicon, vanadium, nickel,

tin

Have effects in the body,

but essentiality is not

established

Fluoride, lithium

May occur in foods and

known to be toxic in excess

Aluminum, arsenic,

antimony, boron, bromine,

cadmium, cesium,

germanium, lead, mercury,

silver, strontium

12 chapter 1

the thyroid gland), is widespread in inland upland

areas over limestone soil. This is because the soil

over limestone is thin, and minerals, including

iodine, readily leach out, so that locally grown

plants are defi cient in iodine. Near the coast, sea

spray contains enough iodine to replace these

losses. Worldwide, many millions of people are at

risk of defi ciency, and in parts of central Brazil, the

Himalayas, and central Africa, goiter may affect

more than 90% of the population. A contributory

problem, in addition to low dietary iodine, may

be the presence of goitrogens (compounds that

interfere with iodine metabolism) in some foods.

Thyroid hormones regulate metabolic activity, and

people with thyroid defi ciency have a low meta-

bolic rate, and hence gain weight readily. They

tend to be lethargic and have a dull mental apa-

thy. Children born to iodine-defi cient mothers

are especially at risk, and more so if they are then

weaned onto an iodine-defi cient diet. They may

suffer from very severe mental retardation (goi-

trous cretinism) and congenital deafness (Institute

of Medicine, 2001).

Apart from iron and iodine, mineral defi ciencies

are likely to be a problem only for people whose

food comes entirely or largely from a limited

region where the soil may be defi cient. For peo-

ple whose food comes from a number of different

regions of the world, mineral defi ciencies are rela-

tively uncommon. Selenium intake in the United

Kingdom has fallen over the last three decades as a

result of increasing use of wheat grown in Europe,

where soils are relatively poor in selenium, com-

pared with earlier use of wheat from Australia

and North America, where soils contain more sele-

nium. Indeed, in some parts of the United States

soils contain so much selenium that grazing live-

stock suffer from selenium poisoning (Rayman,

1997, 2000).

The availability of minerals from foods also

presents a problem. Requirements are estimated from

balance and other studies, using crystalline mineral

salts. However, while chemical analysis reveals the

content of a mineral in a food, much of this may not

be available for absorption. Interactions between

different foods can also affect the availability of

minerals for absorption. Tannins in tea chelate iron

essentials for experimental animals maintained on

highly purifi ed diets, but whose metabolic function

is unknown. These ultra-trace minerals are not of

practical importance in human nutrition. Lithium

salts are known to have a pharmacological effect in

the treatment of bipolar psychiatric disease, and fl u-

oride is known to improve bone health and reduce

dental caries, but neither can be considered to be a

dietary essential.

Most minerals are required in milligram or micro-

gram amounts daily to match losses from the body.

In principle, it is easy to determine mineral require-

ments by balance studies—how much is required to

replace urinary and fecal losses? In practice, it is less

simple. Negative calcium balance may be the result

of bone loss (osteoporosis) in old age, and increas-

ing calcium intake may not restore balance, but sim-

ply lead to higher intake and output, but still with

negative balance.

Iron defi ciency anemia is a major problem of

public health worldwide and, together with iodine

and vitamin A, is one of the WHO’s three micro-

nutrient priorities. The absorption of dietary iron is

strictly controlled by the state of body iron reserves,

because there is no mechanism for iron excretion.

However, excessive blood losses (as in menstrua-

tion or as a result of intestinal parasites) lead to

requirements for replacement that cannot readily

be met from the diet. As a result of menstrual blood

losses, most women between menarche and meno-

pause have negligible body iron reserves, while

men have relatively large reserves. Postmenopaus-

ally, women’s iron reserves increase, approaching

those of men. A further problem of iron nutrition

is that perhaps 10% of the population (and more

in some ethnic groups) are at risk of iron overload

because of genetic polymorphisms in the various

enzymes and proteins involved in iron homeosta-

sis. Iron overload (hemochromatosis) leads to liver

cirrhosis, cardiomyopathy, and pancreatic damage

(bronze diabetes) and can also lead to depletion

of vitamin C as a result of nonenzymic reactions,

and hence the development of scurvy (Institute of

Medicine, 2001).

Iodine is required for the synthesis of the thyroid

hormones, thyroxine and tri-iodothyronine. Defi -

ciency, leading to goiter (a visible enlargement of

h u m a n n u t r i t i o n 1 3

of normal metabolic integrity and homeostasis. In

order to be considered a vitamin, a compound must

be shown to be a dietary essential and have a meta-

bolic function; deprivation must lead to more or less

specifi c defi ciency signs that are reversed by restor-

ing the vitamin to the diet. Table 1.9 shows the vita-

mins and their principal metabolic functions and

defi ciency signs.

For a vitamin or any other nutrient, there is a

range of intakes between that which is clearly

and phytates in unleavened breads chelate calcium

and zinc, reducing their absorption.

Vitamins

Vitamins are organic compounds (and hence dis-

tinct from minerals) that are required in the diet in

small amounts (milligrams or micrograms daily, as

opposed to essential amino and fatty acids, which

are required in gram amounts) for the maintenance

Table 1.9 The vitamins

Vitamin Functions Defi ciency disease

A Retinol,

β-carotene

Visual pigments in the retina, regulation of

gene expression, and cell differentiation

Night blindness, xerophthalmia,

keratinization of skin

D Calciferol Maintenance of calcium balance, enhances

intestinal absorption of Ca2+, and mobilizes

bone mineral

Rickets = poor mineralization of bone,

osteomalacia = bone demineralization

E Tocopherols,

tocotrienols

Antioxidant, especially in cell membranes Extremely rare—serious neurological

dysfunction

K Phylloquinone,

menaquinonesCoenzyme in the formation of γ-carboxy-

glutamate in proteins of blood clotting and

bone matrix

Impaired blood clotting, hemorrhagic

disease

B1 Thiamin Coenzyme in pyruvate and 2-oxoglutarate

dehydrogenases and transketolase, role in

nerve conduction

Peripheral nerve damage (beriberi) or

central nervous system lesions (Wernicke–

Korsakoff syndrome)

B2 Ribofl avin Coenzyme in oxidation and reduction

reactions, prosthetic group of fl avoproteins

Lesions of corner of mouth, lips, and

tongue, seborrheic dermatitis

Niacin Nicotinic acid,

nicotinamide

Coenzyme in oxidation and reduction

reactions, functional part of NAD and NADP

Pellagra—photosensitive dermatitis,

depressive psychosis

B6 Pyridoxine,

pyridoxal,

pyridoxamine

Coenzyme in transamination and

decarboxylation of amino acids and

glycogen phosphorylase, role in steroid

hormone action

Disorders of amino acid metabolism,

convulsions

Folic acid Coenzyme in transfer of one-carbon

fragments

Megaloblastic anemia

B12 Cobalamin Coenzyme in transfer of one-carbon

fragments and metabolism of folatePernicious anemia = megaloblastic anemia

with degeneration of the spinal cord

Pantothenic

acid

Functional moiety of CoA and acyl carrier

protein in fatty acid metabolism and

synthesis

Peripheral nerve damage (burning foot

syndrome)

H Biotin Coenzyme in carboxylation reactions in

gluconeogenesis and fatty acid synthesis

Impaired fat and carbohydrate

metabolism, dermatitis

C Ascorbic acid Coenzyme in hydroxylation of proline and

lysine in collagen synthesis, antioxidant,

enhances absorption of iron

Scurvy—impaired wound healing, loss of

dental cement, subcutaneous hemorrhage

14 chapter 1

protein rather than defi ciency of the nutrient

itself.

• Low urinary excretion of the nutrient, refl ecting

low intake and changes in metabolic turnover.

• Incomplete saturation of body reserves.

• Adequate body reserves and normal metabolic

integrity.

• Possibly benefi cial effects of intakes that are more

than adequate to meet requirements—the promo-

tion of optimum health and life expectancy.

Having decided on an appropriate criterion of

adequacy, requirements are determined by feeding

volunteers an otherwise adequate diet, but lack-

ing the nutrient under investigation, until there is

a detectable metabolic or other abnormality. They

are then repleted with graded intakes of the nutri-

ent until the abnormality is just corrected. Prob-

lems arise in interpreting the results, and therefore

defi ning requirements, when different markers

of adequacy respond to different levels of intake.

This explains the difference in the tables of refer-

ence intakes published by different national and

international authorities (see Tables 1.10, 1.11, 1.12,

and 1.13).

Dietary Reference Values

Individuals do not all have the same requirement

for nutrients, even when calculated on the basis of

body size or energy expenditure. There is a range

of individual requirements of up to 25% around the

mean. Therefore, in order to set population goals

and assess the adequacy of diets, it is necessary to

set a reference level of intake that is high enough to

ensure that no one will either suffer from defi ciency

or be at risk of toxicity.

As shown in the upper graph in Figure 1.3, if it is

assumed that individual requirements are normally

distributed around the observed average require-

ment, then a range of ±2 × the standard deviation

(SD) around the mean will include the requirements

of 95% of the population. This 95% range is conven-

tionally used as the “normal” or reference range

(e.g., in clinical chemistry to assess the normality or

otherwise of a test result) and is used to defi ne three

levels of nutrient intake:

inadequate, leading to clinical defi ciency disease,

and that which is so much in excess of the body’s

metabolic capacity that there may be signs of tox-

icity. Any excess of the water-soluble vitamins is

generally excreted in the urine, but the fat-soluble

vitamins may accumulate in tissues with harmful

consequences. Between these two extremes is a level

of intake that is adequate for normal health and the

maintenance of metabolic integrity, and a series of

more precisely defi nable levels of intake that are

adequate to meet specifi c criteria, and may be used

to determine requirements and appropriate levels of

intake. In order of decreasing severity, or increasing

sensitivity as markers of adequacy, these are

• Clinical defi ciency disease, with clear anatomical

and functional lesions, and severe metabolic dis-

turbances, possibly proving fatal. Prevention of

defi ciency disease is a minimal goal in determin-

ing requirements.

• Covert defi ciency, where there are no signs of

defi ciency under normal conditions, but any

trauma or stress reveals the precarious state of the

body reserves and may precipitate clinical signs.

For example, an intake of 10 mg of vitamin C per

day is adequate to prevent clinical defi ciency, but

at least 20 mg per day is required for healing of

wounds.

• Metabolic abnormalities under normal condi-

tions, such as impaired carbohydrate metabolism

in thiamin defi ciency or excretion of methyl-

malonic acid in vitamin B12 defi ciency.

• Abnormal response to a metabolic load, such as

the inability to metabolize a test dose of histidine

in folate defi ciency or tryptophan in vitamin B6

defi ciency, although at normal levels of intake

there may be no metabolic impairment.

• Inadequate saturation of enzymes with (vitamin-

derived) coenzymes—this can be tested for three

vitamins, using red blood cell enzymes: thiamin,

ribofl avin, and vitamin B6.

• Low plasma concentration of the nutrient, indi-

cating that there is an inadequate amount in tissue

reserves to permit normal transport between

tissues. For some nutrients, such as vitamin A,

this may refl ect failure to synthesize a transport