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Nutrition in Early Life

Edited by

Jane B. Morganand

John W. T. Dickerson

School of Biomedical and Life Sciences

University of Surrey, Guildford, UK

Innodata0470857927.jpg


Edited by

Jane B. Morganand


School of Biomedical and Life Sciences

University of Surrey, Guildford, UK

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Library of Congress Cataloging-in-Publication Data

Nutrition in early life : concepts and practice / edited by Jane Morgan & J.W.T. Dickerson.p. ; cm.

Includes bibliographical references and index.ISBN 0-471-88064-7 (alk. cased)ISBN 0-471-49624-3 (alk. paper)

1. Infants — Nutrition. 2. Children — Nutrition. I. Morgan, Jane. II. Dickerson, John W.T.[DNLM: 1. Infant Nutrition. 2. Child Nutrition. WS 115 N9838 2002]

RJ216.N8585 2002612.3’083 — dc21 2002033050

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CONTENTS

Preface xiii

Foreword xv

List of Contributors xvii

1: Growth, development and the chemical composition of the body 1John W. T. Dickerson

Learning outcomes 1Introduction 1

Growth curves 3Developmental age and physiological maturity 4Factors that influence growth and development 6

Body composition 7Methods for determining whole body composition 8The composition of the whole body 9Composition of the newborn of different species 13

Effects of dietary deficiencies and excess 14Protein-energy deficiency 14Dehydration 15Sodium chloride excess 15Iron deficiency 15

Changes in organ and tissue proportions during growth 16The composition of organs and tissues 17

Skeletal muscle 17The skeleton 21The skin 24Hair 26The liver 26The brain 28

Contribution of major soft tissues to total amounts of body constituents during growth 33

Conclusion 34

2: Pre- and periconceptual nutrition 39Jane Coad

Learning outcomes 39

Introduction 39The relationship between body size and reproductive potential 40

The onset of puberty and body size 40The role of leptin in reproductive function 42

Effect of body weight on reproductive success 47Undernutrition 47Dietary fluctuations, metabolism and reproduction 50Vegetarianism 50Obesity 51Weight loss 51Optimal body mass index 52

Effects of body weight on male reproductive function 52Quality of diet 53

Protein intake 53Micronutrients 54Folate 55Other micronutrients 61

Lifestyle choices and fertility 62

Adolescent pregnancy 63Conclusion 63

3: Maternal physiology and nutrition during reproduction 73Elisabet Forsum


Introduction 73Hormonal changes 74Metabolic changes 76Physiological changes 77

Changes in body weight during reproduction 79Pregnancy 79Lactation 82Composition of weight gained and lost during reproduction 82

Nutritional needs during reproduction 84Assessment of human nutritional requirements 84Energy 84Protein 86Vitamins and minerals 87

Conclusion 88

4: Physiological and nutritional aspects of the placenta 91Michael E. Symonds, Helen Budge and Terence Stephenson


Comparative aspects of fetal growth and maturation 93Placental function and its role in nutrient transfer to the fetus 95Effect of altered nutrition during pregnancy on placental and fetal weight at term 96

Determination of the nutritional requirements of the placenta and fetus 100Hormone secretion by the placenta and regulation of fetal growth 102Placental hormone catabolism 104

Development of fetal organs necessary for metabolic homeostasis after birth 105Skeletal muscle development 106

Nutritional manipulation of skeletal muscle development 107Nutritional requirements of skeletal muscle 108

Adipose tissue development 108Endocrine regulation of adipose tissue maturation in sheep 108Nutrient requirements for adipose tissue growth 109Adipose tissue growth in fetuses adapted to nutritional restriction or enhancement 110

Liver development 113Liver development in fetuses adapted to nutritional restriction or enhancement 115

Conclusion 115

5: Lifestyle and maternal health interactions between mother and fetus 123Mohammed Ibrahim and J. Stewart ForsythLearning outcomes 123

vi CONTENTS

Introduction 123Lifestyle interactions between mother and fetus 124

Diet 124Overweight and obesity 124Tobacco smoking 126Alcohol 126Drug therapy during pregnancy 127Drug–nutrient interactions 128Epilepsy and antiepileptic drugs during pregnancy 128Narcotic drug addiction during pregnancy 129Caffeine 131

Maternal health interactions between mother and fetus 131Anaemia 131Hypertension 132Diabetes mellitus 132Allergy 134Asthma 136Cystic fibrosis and pregnancy 137Systemic lupus erythematosus and pregnancy 137

Conclusion 138

6: The fetus at birth: maternal and fetal preparationsfor postnatal development 145Mary McNabb


Introduction 145Transition from fetal to neonatal metabolism 146Digestion and metabolism in human pregnancy 147

Maternal, placental and fetal metabolism 147Maternal glucose and lipid metabolism 148Placental metabolism of glucose 149Placental metabolism of lipids 149

Interrelationship between the liver and mammary gland 149Placental transport of ketones 151Fetal metabolism – glycogenesis and lipogenesis 151

Feto-placental regulation of metabolism 152Developmental changes in the fetal pancreas 152

Morphological development of pancreatic b-cells 153Insulin and glucagon during fetal and early neonatal development 154

Developmental characteristics of glucagon 155

Hormonal regulation of maternal nutrient metabolism during pregnancy and labour 156Maternal oxytocin from pregnancy to lactation 158Prolactin, GH-V and oxytocin – maternal appetite and metabolism in labour 160Oxytocin, food intake and gastro-intestinal function 161Oxytocin, glucose homeostasis and adipose tissue metabolism 162Maternal and neonatal glucose 165

Fetal neurohormonal responses to labour and birth 165Hormonal regulation of suckling metabolism 167

Maternal hypothalamic–pituitary–adrenocortical axis and oxytocin – influences onneonatal metabolic adaptations 168

Placental corticotrophin-releasing hormone 169Hyporesponsiveness of the maternal HPA axis during pregnancy and labour 169

Conclusion 170

CONTENTS vii

7: Fetal, infant and childhood growth and adult health 179Keith M. Godfrey and David J. P. Barker


Introduction 179Programming and the ‘fetal origins’ hypothesis 179Fetal growth and cardiovascular disease 180

Infant and child growth and coronary heart disease 182Confounding variables 184

Hypertension 185Placental size and blood pressure 185Mother’s blood pressure 186Childhood growth 186Renin–angiotensin system 186Renal structure 187Endocrine 187Vascular structure 187Nervous system 188

Non-insulin-dependent diabetes 188Size at birth and non-insulin-dependent diabetes 188Insulin resistance 189Mechanisms 190Insulin deficiency 191Serum cholesterol and blood clotting 192

Fetal nutrition 192Maternal influences on fetal nutrition 193

The fetal growth trajectory 194Intergenerational effects 194Placental size and transfer capabilities 195Effects on specific fetal tissues 196Maternal diet and body composition 197

Responses to adult living standards 198Conclusion 199

8: Nutrition in infancy 205Lawrence T. Weaver and Ann Prentice


Mammary gland and lactation 207Comparative aspects 207Human mammogenesis 212Human lactogenesis 213Human lactation 214Human mammary gland involution 216

Composition of human milk 217General composition 217Fat 217Carbohydrate 218Protein 218Micronutrients 219Non-nutritional components 220Changes in milk composition during lactation 221

Energy and nutrient requirements 223Alternatives to human milk 224

viii CONTENTS

Animal milks 225Commercial infant formula milks 226

Breast-feeding and health 227Health advantages to the infant 227Health advantages to the mother 229

Conclusion 230

9: Complementary feeding for the full-term infant 233Nilani Sritharan and Jane B. Morgan


Definitions 234Historical trends 234Growth 235

Age of introduction of complementary feeding 236Current recommendations 239

Nutrient profile of complementary foods 240Dietary energy 240Dietary energy recommendations 241Dietary fat 241Dietary fat recommendations 243Non-starch polysaccharide 245NSP recommendations 245Protein 246

The types of complementary foods 246Commercial vs home-prepared foods 247Suitable complementary foods 248Timetable for introducing complementary foods 250

Good infant feeding practices 250Parental misconceptions 250A public health approach 251

Conclusion 253

10: Nutrition of the low-birth-weight and very-low-birth-weight infant 257Caroline King and Michael Harrison


Enteral nutrition 258Requirements 258

Energy 258Protein 259Composition of weight gain 259Lipids 259Vitamin A 259Vitamin D 260Vitamin E 260Water-soluble vitamins 260Calcium, phosphorus and magnesium 260Iron 261Zinc 261Selenium 261

Conditionally essential nutrients 262b-Carotene 262Nucleotides 262Glutamine 262

CONTENTS ix

Type of feed 262Human milk 262Donor milk 263

Nutritional adequacy of human milk 263Energy 263Protein 263Lipids 264Vitamins 264Minerals 264Breast milk fortifiers 265Preterm formulas 265Nutrient-enriched postdischarge formulas 269

Initiation of enteral feeds 269Parenteral nutrition 271Indications for initiation 271

Nutrient composition 271Energy 271Carbohydrate 272Lipids 272Amino acids 272Vitamins 273Minerals and trace elements 273

Future developments 273Glutamine 273Carnitine 273Inositol 274

Monitoring tolerance 274Complications 274Transition to enteral feeding 274

Failure to thrive and catch-up growth 274Diagnosis of failure to thrive 278Causes of failure to thrive 278

Treatment of failure to thrive 279Growth assessment 280

Weight 280Head circumference 280Length 283

Growth charts 283

Conclusion 283

11: Nutrition in childhood 291Elizabeth Poskitt


Age-related changes in body composition relevant to nutrition 291Puberty 293

Assessment of nutritional status 294Issues relevant to development and dietary needs 296

Nutritional requirements and growth rates 296Direction of desirable dietary change 297Food choices 298Milk in children’s diets 299

Nutritional problems in young children 299Fussy eaters 300

x CONTENTS

Macronutrient deficiency and excess 300Failure to thrive 300Emotional deprivation 301Nutritional stunting 302Role of protein-energy deficiency in problems of growth and development,

especially in relation to neurological impairment 302Obesity 303

Macronutrient deficiencies 305Iron deficiency anaemia 307Zinc deficiency 311Iodine deficiency 312Calcium nutrition 314Vitamin D deficiency and rickets 315

Conclusion 317

12: Practical advice on food and nutrition for the mother, infant and child 325Margaret Lawson

Learning outcomes 325Introduction 326Preconception, pregnancy and lactation 328

Rationale for policy 328Practical measures 328

Feeding the infant 335Rationale for policy 335Breast-feeding 336Formula-feeding 338Combined breast- and formula-feeding 340Other milks 340Drinks other than milk 340Weaning 340Vitamins 344Iron 346Minerals and trace elements 347

Problems associated with feeding infants and young children 347Rationale for nutrition policy 347Colic 349Acute diarrhoea 350Vomiting, posseting and gastro-oesophageal reflux 350Constipation 351Food intolerance and allergy 352Failure to thrive 353

Feeding children aged 1–5 years 356Rationale for nutrition policy 356Cultural influences on diet 356Fussy eaters 357Healthy eating recommendations for pre-school children 358

School-age children 359Rationale for nutrition policy 359

Adolescents 360Rationale for nutrition policy 360

Obesity 361Rationale for nutrition policy 361

Conclusion 363

Index 366

CONTENTS xi

PREFACE

The developing bodies of multicellular organ-isms are in a condition of ‘plasticity’, forchanges in structure and function are continu-ally taking place. There is a harmony in theseprocesses as the multitude of changes asso-ciated with growth and development areinterdependent and time-related. Moreover,the various processes are subject to moderationand control by genetic, nutritional, hormonaland other influences.Each of us, the Editors, of the present book,has had an extensive interest over a long periodof time in aspects of growth and developmentin both teaching and research. In these activ-ities we drew considerable inspiration and helpfrom a book, Developmental Nutrition byLucille Hurley published in 1980. This bookis now out of print and out of date. Moreover,increase in knowledge and the recognition ofthe importance of developmental aspects ofnutrition in the training of health professionalspointed to the need for an up-to-date andextended text incorporating scientific aspects ofthe subject and their practical application. Therecognition that disturbances in biochemicalprogramming during development, resulting inaberrations of the normal harmony of growth,can influence the development of disease laterin life provided a further incentive. The seedsof much that is in the book can be traced backto the work of R. A. McCance FRS and E.Widdowson FRS in the 1950s and 1960s. Tothem we would like to dedicate the book.We have tried to trace the development of

the human organism from the time when this

can be investigated in the fetus through tomaturity. We have approached the subjectfrom structural, physiological and nutritionalstandpoints through to the application of thesescientific principles in the feeding of babies andchildren. Also, we have recognized that thenutrition of the mother is central to theadequate provision of care and nutrition forinfants at particular times in their lives. Indeveloping these themes we have had torecognize that certain aspects of the subjectare not amenable to direct observation ormeasurement in mothers and babies andalternative sources of information have hadto be used.We are grateful to our colleagues who have

shared our enthusiasm for the theme of thebook and have generously contributed to it intheir particular field of interest. With twoexceptions the authors are currently located inthe UK, and this has led inevitably to the texthaving a UK focus. If the focus had beenextended this would have resulted in a largerbook with the danger of taking it beyond ourprime aim, the provision of a student textbook.We are deeply grateful to our publishers,

John Wiley and Sons, for their unstintingsupport of this venture and we are particularlygrateful to Nicky McGirr for her help in somany ways.

Jane B. Morgan and John W.T. DickersonBrook, Surrey

April 2002

FOREWORD

The effects of nutrition and nutritional stressdepend on a triad of influences, the genes of anindividual, the stage of development he or shehas reached and the circumstances in whichthey live. This book describes the middle factorof the triad. If we take folic acid as an examplethen, depending on the stage of development,the effects of its presence or absence in the dietwill vary from a neural tube defect duringorganogensis, to megaloblastic anaemia inpregnancy or malabsorption, cardiovasculardisease due to homocystinaemia in middle age,and precipitation of spinal cord disease bymasking the haematological clues to vitaminB12 deficiency in older people.Conventional textbooks of nutrition describein great detail the situation for healthy adults.They then dispose of the developmentalaspects with a few added chapters on so called‘vulnerable groups’ such as children, pregnantwomen and older people. This book thereforecomes as a breath of fresh air with itsdevelopmental approach acknowledging thatall individuals are either going through or havepreviously experienced various stages of devel-opment – hardly special vulnerable groups butrather the whole population.

The editors are well versed in the develop-mental approach – Morgan from her studiesof dietary intake, in particular energy, andtheir effects on growth, initially in London andSouthampton, and Dickerson from his studiesof normal and retarded growth on bodycomposition, initially in Cambridge and Lon-don. They came together at the University ofSurrey and began a fruitful collaboration,including the concept and organization ofthis book. The authors are committed to theview that nutrition plays a vital role in growthand development throughout the entire lifecycle. The contents of this book are aninterpretation of this view. They, and theirdistinguished panel of contributors, describethe crucial role of biological age and develop-mental clocks in the nutritional health ofpeople.

Professor Brian WhartonHonorary Professor of

University College LondonMRC Childhood Nutrition Research Centre

Institute of Child HealthGuilford StreetLondon, UK

LIST OF CONTRIBUTORS

David J.P. Barker, MRC Environmental Epidemiology Unit, Southampton General Hospital,Southampton, UK

Helen Budge, Academic Division of Child Health, School of Human Development, UniversityHospital, Nottingham, UK

Jane Coad, European Institute for Health and Medical Sciences, University of Surrey, Guildford,UK.Current address: Institute of Food, Nutrition and Human Health, Massey University,Palmerston North, New Zealand

John W.T. Dickerson, School of Biomedical and Life Sciences, University of Surrey, Guildford,UK

Elisabet Forsum, Division of Nutrition, Department of Biomedicine and Surgery, University ofLinköping, Linköping, Sweden

J. Stewart Forsyth, Tayside Institute of Child Health, University of Dundee, Dundee, UK

Keith M. Godfrey, MRC Environmental Epidemiology Unit, Southampton General Hospital,Southampton, UK

Michael Harrison, Department of Paediatrics and Neonatal Medicine, Hammersmith Hospital,London, UK

Mohammed Ibrahim, Tayside Institute of Child Health, University of Dundee, Dundee, UK

Caroline King, Department of Nutrition and Dietetics, Hammersmith Hospital, London, UK

Margaret Lawson, MRC Childhood Nutrition Research Centre, Institute of Child Health,London, UK

Mary McNabb, Division of Midwifery, South Bank University, London, UK

Jane B. Morgan, School of Biomedical and Life Sciences, University of Surrey, Guildford,UK

Elizabeth Poskitt, Public Health Nutrition Unit, London School of Hygiene and TropicalMedicine, London, UK

Ann Prentice, MRC Human Nutrition Research, Elsie Widdowson Laboratory, Cambridge, UK

Nilani Sritharan, School of Biomedical and Life Sciences, University of Surrey, Guildford, UK.Current address: The Dairy Council, 5–7 John Princes Street, London, UK

Terence Stephenson, Academic Division of Child Health, School of Human Development,University Hospital, Nottingham, UK

Michael E. Symonds, Academic Division of Child Health, School of Human Development,University Hospital, Nottingham, UK

Lawrence T. Weaver, Department of Child Health, Royal Hospital for Sick Children, Universityof Glasgow, UK

xviii CONTRIBUTORS

1GROWTH, DEVELOPMENT AND

THE CHEMICAL COMPOSITION OF

THE BODY


LEARNING OUTCOMES

. Knowledge of the mechanisms of growth, and how it can be measured andrecorded.

. How to assess developmental age and the factors that a¡ect it.

. How the chemical composition of the body changes before and after birth.

. How the composition of organs and tissues changes during growth and develop-ment.

. What e¡ects protein-energy malnutrition has on growth and development.

Introduction

Growth and development are the processes bywhich the fertilized ovum is transformed into amature individual. Growth occurs by cell

multiplication (hyperplasia), by cell enlarge-ment (hypertrophy) and by the synthesis ofextracellular tissue. This latter process includesan expansion of the volume of extracellularfluid and an increase in the amounts of specific,

but diverse proteins such as those in the plasmaand the organic matrix of the skeleton. In mostorgans, cell multiplication ceases at a tissue-specific age and further growth is by enlarge-ment of existing cells (Winick and Noble,1965). We can measure the number of cells inan organ which has only mononuclear diploidcells by measuring the amount of DNA in theorgan and dividing this by the amount of DNAin a diploid nucleus, which is about 6.2 pg.Changes in the size of cells can be estimatedfrom the ratio of the amount of proteinassociated with a diploid nucleus or, to put itsimply, by the protein/DNA ratio. Cell multi-plication continues throughout life in the hairfollicles, the epidermis and the mucosa of thealimentary tract. Increase in body fat does notconstitute growth, although it may greatlyincrease body weight. The synthesis of newtissue uses energy and the energy cost of weightgain has been calculated to be 4.6 kJ/g afterdeducting the energy stored (Passmore andEastwood, 1986).

Development constitutes those changes instructure, function and composition which arean essential part of the maturation process.Growth and development are complex, inte-grated processes that are closely related to timeand are dependant on appropriate nutrition(McCance, 1962). If the food supply is reducedat an early age, including early postnatal life,growth and development are separated fromtime and are retarded in ways that are organ-and tissue-specific. Following such a period ofgrowth retardation due to malnutrition orsevere illness, nutritional rehabilitation isaccompanied by a period of ‘catch-up’ growthduring which the growth velocity is greaterthan normal for the age of the child. Themagnitude of the increase in growth velocitydepends on the age of the child and the severityand duration of the growth retardation. It maybe as much as twice the normal velocity inyoung children with prolonged retardation.The ability of a malnourished animal or childthen to return to its normal growth trajectory

depends on the magnitude of the catch-upgrowth. The biological basis for failure of‘catch-up’ growth to return the individual tothe normal trajectory for the individual is atpresent not clear. An early hypothesis that it isdue to a reduction in the period of hyperplasticgrowth has not been confirmed in the rat(Sands et al., 1979).The growth curve of the whole body and of

its constituent parts has a sigmoid shape, butdifferent organs and tissues grow at differentrates and at different times. The four maintypes of growth curve are shown in Figure 1.1(Tanner, 1962; from Scammon, 1930). Theperiod of rapid increase in the ‘General’ curve

2 GROWTH, DEVELOPMENT AND THE CHEMICAL COMPOSITION OF THE BODY

Figure 1.1 Growth curves of different parts andtissues of the body. All the curves are of size attainedand plotted as percentages of total gain from birth to

20 years so that size at age 20 is 100 on the verticalscale. Data from Scammon [reproduced by permissionof Blackwell Science from Tanner (1962) Growth at

Adolescence, 2nd edn].

from about 12 to 15 years is called the ‘adoles-cent spurt’ and involves every muscular andskeletal dimension in the body. Maturity is notachieved until this has been completed, andagain this is related to time and is separatedfrom time by nutritional deprivation. The earlyrapid growth of the head and brain shown inFigure 1.1 is an example of a ‘growth gradient’,and this particular one is called the ‘cephalo-caudal’ gradient. The head of a young childmay be almost the same size as that of itsmother. The changes in the relative size ofdifferent parts of the body with growth anddevelopment are also shown in Table 1.1, inwhich the sizes of different parts of the bodyare expressed as a percentage of the total bodylength. The proportion accounted for by thehead and neck decreases from approximately30 per cent in the 5-month-old fetus toapproximately 12 per cent in the adult. Incontrast, the percentage of length accountedfor by the lower limbs increases from approxi-mately 24 per cent in the fetus to 43 per cent inthe adult. The percentage of the body lengthcontributed by the trunk (about 40 per cent)hardly changes during growth. In the leg,another gradient may be distinguished, asgrowth in foot length ceases before that ofthe calf, and that of the calf before that of thethigh. Material in Chapters 2 and 7 should beread in relation to this chapter.

Growth curves

Each individual has his or her own growthcurve, or ‘trajectory’, as it is called, if measuredlongitudinally. The oldest such curve is that ofa boy measured every 6 months for 18 years byCount de Montbeillard (Figure 1.2; fromTanner, 1962). The longitudinal construction

INTRODUCTION 3

Table 1.1 Relative lengths (percentage) of parts ofthe human body during growth; values calculated from

Medawar (1944) (from Tanner, 1962)

Age

(years)a Head Trunk

Upper

limbs

Lower

limbs

0.42 33 43 26 24

2.75 21 41 34 376.75 16 41 34 4125.75 12 43 37 43

aAge from 5 months postconception.

Figure 1.2 Growth in height of de Montbeillard’sson from birth to 18 years, 1759–1777. Top, distancecurve, height attained at each age; bottom, velocity

curve, increments in height from year to year. Datafrom Scammon [reproduced by permission ofBlackwell Science from Tanner (1962) Growth at

Adolescence, 2nd edn]

of such growth curves for individual children isof considerable value in clinical paediatrics.There are many causes of growth failure, or‘failure to thrive’, one of which is malnutrition;the construction of an individual child’sgrowth curve permits the degree of growthfailure to be assessed and the progress ofrehabilitation to be followed. To help in thisprocess, standard growth curves, and particu-larly percentile charts, have been constructedfrom measurements of large numbers of chil-dren of different ages, that is from cross-sectional measurements. In percentile charts(Figs 10.2a–d, the height or weight, or what-ever other measurement is being considered,follows the 50th percentile for 50 per cent ofthe children measured at a particular age.Similar percentiles are drawn in such a waythat a greater or a smaller number of childrenhave values below the line. Ideally, growthcharts should be available nationally in differ-ent countries. Perhaps the best known arethose for the USA (Hamill et al., 1977), and inthe UK the curves produced by Tanner et al.(1966) have been replaced by those publishedby Freeman et al. (1995). It is often some timeafter the measurements were made before thecharts become available. Thus, the US chartsare based on data collected between 1929 and1975 and Tanner et al.’s UK charts were basedon data collected between 1952 and 1954. Thisposes a problem if infant feeding practiceschange as this might result in changes in infantand children’s growth rates. Differences ininfant feeding practices, for instance, in devel-oping countries, suggest that growth chartsshould be kept under review (Whitehead andPaul, 2000). Prentice (1998) has suggestedusing body mass index (BMI; defined asweight/height2, kg/m2) charts available fromthe Child Growth Foundation (LondonW4 1PW, UK) for the assessment of nutri-tional status in children. Cole (2001) hasdiscussed the use and abuse of centile curvesfor the BMI. The application of BMI charts tochildren was first suggested by Cole (1979).

Developmental age andphysiological maturity

The age of a child can be expressed in two ways.It is usually quoted simply as the number ofyears, months or weeks since it was born. This isits ‘chronological’ age. Then we can also deter-mine its ‘developmental’ age, which is ameasureof how far the child has progressed towardsmaturity. This can be assessed in a number ofdifferent ways (Table 1.2). Each method hasits own limitations and it is necessary toconsider each method in some detail.Skeletal age is the most commonly used

indicator of physiological maturity (Tanner,1962). It is a measure of the degree of develop-ment of the skeleton as measured by theappearance and size of the epiphyses of certainbones. Each bone begins with a primary centreof ossification. It then enlarges, changes shapeand secondary centres of ossification developin the cartilaginous epiphyses. Eventually, theepiphyses fuse and the epiphysial plate dis-appears. This sequence of changes is the samefor all indivduals, whatever the rate of devel-opment. Skeletal maturity is judged both onthe number of centres present and on the stageof development of each. The appearance of theepiphyses at birth may differ from one child toanother with different numbers of primarycentres developed and larger areas ossified.Areas of ossification are not of themselvesconsidered good indicators of bone develop-ment as they differ according to the size of theindividual.Assessment of skeletal maturity is accom-

plished by comparing an X-ray with a set of


Table 1.2 Assessment of developmentalage – systems in use (Tanner, 1962)

Skeletal ageDental ageMorphological or shape age

Secondary sex characteristics age

standards. There are two ways of doing this.An older, atlas method involved matching anX-ray with standards representing the ‘norm’for different ages, with a skeletal age beingassigned to a test X-ray according to the age ofthe nearest match in the atlas. Tanner et al.(1961) refined this method by assigning a scoreto different changes in bone maturity. In thismethod, a test X-ray scored a number ofdevelopment points. The bones for which thereare standard atlases are the wrist and the knee,with separate standards for the two sexes. Thisis because girls are more mature at birth,before it and throughout the whole period ofgrowth up to adolescence. It is to be noted thatskeletal age can be assessed throughout theperiod of growth of the bones.Dental age can be obtained using the same

principle as skeletal age, with eruption andnoneruption of teeth as the index correspond-ing to the appearance and non-appearance ofan ossification centre. A refinement of thismethod involves more detailed observationand scoring of degrees of tooth eruption androot development. The use of dental age isclearly limited to the period when the decid-uous and permanent teeth are erupting. Fordeciduous dentition this is from about 6months to 2 years. The corresponding periodfor permanent dentition is from 6 to 13 years.There is a marked sex difference in theeruption of teeth, with all teeth appearingearlier in girls than in boys by an amountvarying from 2 months for the first molars to11 months for the canines (Tanner, 1962). Itmay be considered that the times of theeruption of teeth are just as crude a methodof assessing developmental age as the timing ofthe presence of ossification centres. It has beensuggested that in the absence of a birthcertificate the state of teeth eruption can beused to estimate chronological age. To thisend, published data from 42 studies of chil-dren’s dentition transformed into chronologi-cal age have been examined (Towsend andHammel, 1990). Lack of significant differences

between the estimates of age seemed to justifythe use of a single set of data. However, resultsof a longitudinal study of 129 Finnish childrenbased on deciduous teeth (Nystrom et al.,2000) led to the conclusion that estimates ofage should not be based on teeth eruptionalone because of marked variation in theirhomogeneous group of children.Morphological or shape age has been con-

sidered as a means of assessing development.The idea that changes in shape of the bodymight be quantified and used in this way wasprobably first suggested by Godin in France in1903 (quoted by Tanner, 1962) and was laterdeveloped by Medawar (1944) with referenceto the shape change in vertical proportions (seeTable 1.1). Tanner (1962) quotes Richards andKavanagh (1945) as having outlined the math-ematical procedures by which this might beachieved. The concept seems not to have beenpursued further.Sexual age is derived from observations of

the development of secondary sex character-istics. The adolescent growth spurt, and thedevelopment of these characteristics, occurslater in boys than in girls. The age ranges overwhich the changes begin and end are shown inTable 1.3. A scoring system of 2–5 is used to

INTRODUCTION 5

Table 1.3 The sequence of events at adolescence inboys and girls used to assess developmental age(adapted from Tanner, 1962)

Beginning(years)

End(years)

BoysHeight spurt 10.5–13 16–17.5

Penis growth 11–13.5 14.5–17Testis growth 10–14.5 13.5–18Pubic hair (grades 2–5) 10–14 15–18

Girls

Height spurt 9.5–14.5Menarche 10–16.5Breast (grades 2–5) 8–13

Pubic hair (grades 2–5) 8–14

assess breast development in girls and pubichair in both sexes (Tanner, 1962). Sexualdevelopment, and particularly the age ofmenarche, is occurring earlier now than itwas, say, 100 years ago due to what is calledthe ‘secular trend’ (Wyshak and Frisch,1982). Obviously, the ages over which theseassessments of development can be used arelimited to those ages over which the changesoccur. Key factors which influence their devel-opment are sex hormones and nutrition. In thedisease anorexia nervosa, which occurs mostcommonly in adolescent girls, who are oftenseverely emaciated although secondary sexcharacteristics are usually well developed,amenorrhoea is a common feature. Thisfeature of the disease is closely linked withbody weight (Frisch, 1994).

Factors which in£uence growthand development

The rate of development can be assessed, as wehave seen, by the age at which certain mile-stones of development occur. This age can beaffected by genetic constitution, nutritionalstatus (often associated with poverty), severeillness, psychological disturbance and thesecular trend.

Early observations about the influence ofgenetics pertained to the age of menarche inmothers and daughters (quoted by Tanner,1962). Pairs of identical twins were closest inage of menarche, with an average difference of2.8 months; non-identical twins, with a differ-ence of 12 months, were not very differentfrom sisters (12.8 months), with unrelatedwomen showing a difference of 18.6 months.According to Tanner, evidence of geneticcontrol has also been noted for the reachingof peak growth velocity, skeletal maturity andin the growth of specific muscles. Under-nutrition and, often with it, poverty or faminecan have a profound effect on growth, separ-

ating it from time. The effects may manifestthemselves in the fetus, with the result that thebaby is born ‘small-for-dates’, or after birth,when the child’s growth is stunted. In rats,which are born at an earlier stage of develop-ment than humans, it is easy to show apermanent stunting when the animals arenutritionally deprived at an early age. Inhuman babies, in which there is, by compar-ison, an extended period of growth anddevelopment, it is much more difficult toshow permanent stunting. The greater amother’s size before pregnancy, the more likelyshe is to have a normal birth-weight baby(Naeye, 1981). For women who are under-weight when they conceive, the amount of foodthey consume during pregnancy affects thebirth-weight (Papoz et al., 1981). In motherswith protein-energy malnutrition (PEM), orwho have a preconception daily energy intakeof 7.5 MJ (1800 kcal) or less, appropriate foodsupplementation during pregnancy, dependingon the size of the deficiency, increases fetalgrowth and decreases the number of low-birth-weight babies (Lechtig and Klein, 1981). As tothe effect of supplementation after birth, thefollowing examples will suffice. During thepost-war famine in Europe in 1947–1948,children in a German orphanage whose dietsaveraged about 80 per cent of their desirablenutrient intake were supplemented for a yearwith bread and other foods (see Widdowson,1951). During the period of the supplementtheir heights and weights increased at a greaterthan normal rate (that is they showed ‘catch-up’ growth) and their skeletal maturity chan-ged in parallel with their growth. In a secondexample, a group of 141 Korean girls wereadmitted to the USA and adopted intoAmerican families (Winick et al., 1975). Thegirls were divided into three groups of whom42 were severely malnourished and below the3rd percentile for both height and weight byKorean standards. Another 52 were marginallymalnourished, between the 3rd and 25thpercentile for height and weight, and 47 were


well-nourished and above the 50th percentilefor height and weight. The families whoadopted them before their second birthdayhad no idea of the children’s previous nutri-tional history. By the time they were 7 years ofage there were no differences in the averageweight of the three groups of children althoughthe average height of the previously malnour-ished Korean children remained statisticallybelow those of the well-nourished children. Allthe Korean children remained shorter andlighter than the American standards.Illness only has a transient effect on chil-

dren’s growth unless it is severe; then its effectsmimic those of malnutrition. That the psycho-logical state of children affects the effects offood on body growth was a serendipitusobservation during the supplementation studyin the German orphanages mentioned above(Widdowson, 1951). During the supplementa-tion it was found that it was the presence of aSister (called ‘B’, in the write-up) in theorphanage, rather than the food available,that determined the children’s growth, as themealtimes were chosen by her as an opportu-nity to severely reprimand the majority of thechildren, other than those who were ‘B’sfavourites; it was these favourites who gavethe expected response to the rations. There wasno doubt that the children who did notrespond consumed the supplements.The ‘secular trend’ is the term used to

describe the striking tendency for the age ofadolescence, for example menarche, and thegrowth spurt to take place earlier than they did100 years ago. Similar trends have beenreported in all Western countries. These trendsare greater than the differences between socialclasses (Tanner, 1978). In countries with largepopulations such as India, trends in growthand development may be induced by racial,ethnic and genetic factors as well as thosecaused by socioeconomic status and nutrition.This may make it necessary to construct local/regional growth standards (Singh, 1995). Thesecular trend has had sociological and medical

effects; the latter are shown by the occurrenceof myopia in children at the earlier age ofpuberty (Tanner, 1962).

Body Composition

The composition of themammalian body can beconsidered from three different viewpoints –anatomical, physiological and chemical – eachof which has importance for the nutritionistand implications for public health and clinicalmedicine. Anatomically, our bodies consist ofa number of organs and tissues which con-tribute varying proportions to the total bodyweight. Physiologically, our bodies contain 60–70 per cent water, which is distributed betweenthe cellular and extracellular compartments,with the different composition of the intracel-lular fluid (ICF) and the extracellular fluid(ECF) being maintained by energy-dependentmechanisms in the cell membranes. Also,physiologically, our bodies can be dividedinto energy-expending tissues, collectivelycalled the ‘lean body mass’ (LBM) andenergy-storing adipose tissue, collectivelycalled the ‘fat mass’ (FM). Chemically, thebody consists of various organic and inorganicsubstances that are functionally integrated,with the mineral composition of the bodynecessarily depending on its organic structure.There are nevertheless three factors whichpredominantly affect the proportion of inor-ganic elements in the body and its tissues. Thefirst is the amount of fat, as fatty tissuecontains comparatively little inorganic mate-rial, so that it acts mainly as a diluent. Thesecond is the amount of ECF in the body ortissue at the moment of analysis. Structurallyand functionally this is important in theprocess of development, in which there is adecrease in the volume of ECF consequentupon the increase in the cell mass (CM), and indisease, in which malnutrition produces theopposite changes – an increase in the volume

BODY COMPOSITION 7

of ECF consequent upon a decrease in the CM.The magnitude of the changes in the propor-tion of ECF far outweigh the changes in itscomposition or in that of the cells. The thirdfactor is the amount of bone and its degree ofcalcification, as the adult skeleton contains 99per cent of the body’s calcium. Changes in theconcentration of calcium in the body fluidshave important physiological consequences,but they have no appreciable effect on thecomposition of the body.

It is important to remember, as we discussthe chemical composition of the body, that weare considering a static picture of a dynamicscene, for the molecules of which our bodiesare composed are in a state of individual andcollective activity, and what we are consideringis like a snapshot of a busy street full ofpedestrians and automobiles (Widdowson andDickerson, 1964).

Methods for determining wholebody composition

Chemical analysis

Detailed discussion of the methods availablefor the analysis of the human body is outsidethe scope of this chapter. However, it shouldbe noted that chemical analysis is essentially adestructive process and can be carried out onlyafter death or on tissue obtained by biopsy.Quantitative analysis of whole bodies presentsconsiderable difficulties. In the first place, it isnecessary for the investigator to obtain permis-sion from the relatives or guardians of thebody to deal with it in this way. This is noteasy. It is even more difficult to obtain thebody of a healthy person. This problem,together with that of handling such a largeamount of material in a quantitative fashion,has limited the number of adult human bodiesthat have been analysed. In fact, up to 1945,our knowledge about the chemical composi-tion of the adult human body was derived from

work carried out in Europe about 100 yearsago; since that time the composition of fivemore human bodies (four men and onewoman) has been determined (see Widdowsonand Dickerson, 1964). It is likely that this willremain the total information that we have ofthe elemental composition of the adult humanbody. The bodies of human fetuses and still-born babies are much easier to deal with andthe results of the analysis of these will beconsidered here. Again, though, trends inpublic opinion and ethical considerationsmake it unlikely that there will be any furtheranalyses of this nature. This adds value to thework of Fomon et al. (1982) in producingcalculated data for the composition of ‘refer-ence’ children up to 10 years of age, and thesewill be considered later.

Other methods

There has been, and is continuing to be,research into other methods for the determina-tion of aspects of the composition of the livinghuman body. Much of this development hasstemmed from a concept of the body as con-sisting of two components, fat and lean tissue(Behnke et al., 1942). This is now referred to asthe ‘two-compartment model’ of body compo-sition. A four-compartment model for theassessment of body composition of humanshas been devised which involves the determi-nation of body fat by underwater weighing,total body water (TBW) by deuterium, totalbody mineral by dual-energy X-ray absorptio-metry (DXA) and fat-free body mass as bodyweight minus fat (Fuller et al., 1992). Cowardet al. (1988) reviewed the established techni-ques available at that time: measurement ofbody fat from measurements body density,TBW, total body potassium and determinationof body fatness by anthropometry. They alsoreviewed the newer technique of electricalconductivity and impedence. In a study inwhich body fat was measured in lean and obese


individuals (McNeill et al., 1989) by sixdifferent methods [skinfold thickness, under-water weighing, whole body 40K counting,deuterium dilution of body water, tetrapolarbioelectrical impedence and magnetic reso-nance imaging (MRI)], it was found that,despite high correlations between any twodifferent methods over a wide range of fatness,there was substantial disagreement between theresults by the different methods in the sameindividual. Measurements of gross body fat inrats by DXA, compared with absolute valuesdetermined by carcase analysis (Jebb et al.,1994), showed that this method overestimatedbody fat in the rats by 30–39 per cent. Bio-electrical impedence analysis has been shownto be of greater value in assessing lower limbmuscle area in groups of subjects rather than inindividuals (Fuller et al., 1999). The need forsimple (and preferably inexpensive) methodsfor the determination of aspects of bodycomposition at the bedside has led to researchinto methods that could be used to calibratesuch instruments (Elia and Ward, 1999). TheBOD POD body composition system devel-oped in the US (Life Measurement Systems,Concord, CA, USA) can be used to measurebody volume by air, rather than by water,displacement, as in the method describedby Behnke et al. (1942) for the determinationof body density. This method of determiningbody fat then becomes possible in children.Alternatively, deuterium dilution can bemeasured by infrared spectroscopy rathermore cheaply than by mass spectroscopy.Bioelectrical impedance can be used to accu-rately measure skinfold thickness. Again, boththese methods can be used in children.The main conclusion that can be drawn from

the literature on this subject is that a variety ofexpensive research tools are available whichare essentially difficult to calibrate againstabsolute values. Reproducibility of results,availability, cost and expertise all need to beconsidered in the use of any of them. Thereason for making the measurement also needs

to be considered, whether it is for research orto follow the progress of treatment in a singleindividual. If it is simply a matter of assessing achange in nutritional status, repeated carefulmeasurement of body weight under standardconditions together with triceps skinfold thick-ness may suffice.

The composition of the wholebody

The e¡ect of development

Table 1.4 shows the changes in the chemicalcomposition, determined by chemical analysis,of human fetuses and stillborn babies varyingin weight from 0.75 to 4373 g. The smallest ofthe foetuses contained 924 g of water per kg ofbody tissue, which is about the same amountthat exists in serum after birth. The heavieststillborn baby (4373 g) contained only 585 g ofwater per kg of tissue. Part of the difference inthe amount of water was due to the differencein fat content, 5 g compared with 282 g per kg,and on a fat-free basis the proportion of waterin the body fell from 930 to 820 g per kg ofbody tissue. It is important to note that theamount of fat in the body did not rise above100 g per kg until a fetus weighed more than2600 g and reference will be made to this againlater. When information from other workers isincluded (Figure 1.3), we find that the watercontent of the body falls rapidly during earlygrowth, reaching 880 g per kg fat-free tissuewhen the fetus weighs 50–100 g and thendeclining more gradually to 820 g per kgwhen the fetus reaches full term. This fall inwater content is due to a reduction in theamount of ECF consequent on an increase inthe CM and is reflected in a fall in theconcentrations of the EC ions, sodium andchloride, and a rise in the concentration of thepredominantly intracellular ion, potassium.However, not all the sodium in the body islocated in the ECF and it has been calculated

BODY COMPOSITION 9

that at term about 13 per cent of the body’ssodium is found in the bones and that fromabout the seventh month of prenatal life thefall in the proportion of extracellular sodium isapproximately counter-balanced by increasesin sodium in the skeleton. The skin alsocontains much sodium and chloride at allages and the concentration of chloride in adultskin is at least as high as that in the skin of afull-term baby. The changes in the amount ofcalcium in the body are a reflection of theossification of the skeleton and this begins tooccur when the fetus weighs between 700 and900 g and rises to term. The increase in themineralization of the skeleton also contributes

to the rise in the amount of phosphorus in thebody; the soft tissues also contain phosphorusand thus the increase in the CM also contri-butes to the increase in the body’s content ofthis mineral. The concentrations of iron,copper and zinc in Table 1.4 show littleevidence of regular trends with the progressof gestation.Using information obtained by ‘dilution’

methods, it is possible to extend the develop-mental curve for some body constituents tofind what Moulton (1923) described as the ageof ‘chemical maturity’. Using this information(Widdowson and Dickerson, 1964) it is possi-ble to conclude that total water, ‘exchangeable’


Figure 1.3 Water (g/kg) in the fat-free body tissue of the human foetus during growth [different symbolssignify different sources of data; reproduced fromWiddowson and Dickerson (1964).Mineral Metabolism, Vol. 2A,pp. 1–217, by permission of Academic Press]

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