CONTENTS Cover Title page Preface Acknowledgements About the companion website Abbreviations Glossary of terms used in this book CHAPTER 1: Introduction to lifespan nutrition 1.1 The lifespan approach to nutrition 1.2 The concept of balance 1.3 The individual response to nutrition 1.4 Assessment of nutritional status 1.5 Nutritional epidemiology: Understanding diet–disease relationships 1.6 Dietary reference values References Additional reading CHAPTER 2: Before life begins 2.1 Introduction 2.2 Nutrition and female fertility 2.3 Nutrition and male fertility 2.4 Preparation for pregnancy References Additional reading CHAPTER 3: Pregnancy 3.1 Introduction 3.2 Physiological demands of pregnancy 3.3 Nutrient requirements in pregnancy 3.4 Diet in relation to pregnancy outcomes 3.5 Nausea and vomiting of pregnancy 3.6 Cravings and aversions 3.7 Gastrointestinal disturbances in pregnancy 3.8 High-risk pregnancies References Additional reading CHAPTER 4: Fetal nutrition and disease in later life 4.1 Introduction 4.2 The developmental origins of adult disease 4.3 Evidence linking maternal nutrition to disease in later life 4.4 Mechanistic basis of fetal programming 4.5 Implications of the programming hypothesis References Additional reading CHAPTER 5: Lactation and infant feeding 5.1 Introduction 5.2 The physiology of lactation 5.3 The advantages of breastfeeding 5.4 Trends in breastfeeding behaviour 5.5 Situations in which breastfeeding is not advised 5.6 Alternatives to breastfeeding References Additional reading CHAPTER 6: Nutrition and childhood 6.1 Introduction 6.2 Infancy (birth to five) 6.3 Childhood (5–13) 6.4 Obesity in children References Additional reading CHAPTER 7: Nutrition and adolescence 7.1 Introduction 7.2 Physical development 7.3 Psychosocial development 7.4 Nutritional requirements in adolescence 7.5 Nutritional intakes in adolescence 7.6 Potential problems with nutrition References Additional reading CHAPTER 8: The adult years 8.1 Introduction 8.2 Changing needs for nutrients 8.3 Guidelines for healthy nutrition 8.4 Disease states associated with unhealthy nutrition and lifestyle References Additional reading CHAPTER 9: Nutrition, ageing and the elderly 9.1 Introduction 9.2 The ageing population 9.3 The ageing process 9.4 Nutrient requirements of the elderly 9.5 Barriers to healthy nutrition in the elderly 9.6 Common nutrition-related health problems References Additional reading APPENDIX: An introduction to the nutrients A.1 Classification of nutrients A.2 Carbohydrates A.3 Lipids A.4 Proteins A.5 Micronutients Index End User License Agreement List of Tables Chapter 01 Table 1.1 The acute phase inflammatory response to trauma or infection Table 1.2 The metabolic response to injury and infection increases requirements for energy and protein Table 1.3 The three stages of iron deficiency Table 1.4 Anthropometric measures used to estimate body composition and nutritional status Table 1.5 Advantages and disadvantages of dietary assessment methods Table 1.6 Definitions of key terms in epidemiology Table 1.7 Study designs in nutritional epidemiology Table 1.8 Definitions of dietary reference value terms used in the United Kingdom, North America and Oceania Chapter 02 Table 2.1 Reactive oxygen species and antioxidants in biological systems Table 2.2 Environmental sources of human exposure to endocrine-disrupting chemicals Table 2.3 Organic food, pesticide exposure and semen quality Table 2.4 Factors that impact on parental health during the periconceptual period Chapter 03 Table 3.1 Development of the human organs during gestation Table 3.2 Optimal weight gain for women in pregnancy is dependent upon their prepregnancy BMI Table 3.3 Risk factors for preterm delivery Table 3.4 Pica behaviours Table 3.5 US Institute of Medicine recommendations for micronutrient supplementation in multiple pregnancy Chapter 04 Table 4.1 The classical actions of glucocorticoids Chapter 05 Table 5.1 The composition of human milk Table 5.2 UK reference nutrient intakes (RNI) for lactating women Table 5.3 The health benefits of breastfeeding for women and their babies Table 5.4 Definitions of breastfeeding behaviour Table 5.5 Ten steps to successful breastfeeding Table 5.6 Comparison of full-term and preterm infant formula composition (selected nutrients) Chapter 06 Table 6.1 Developmental milestones for infants Table 6.2 A comparison of nutrient requirements* between adults and children under the age of 5 years Table 6.3 Complementary feeding stages Table 6.4 Energy requirements of children Table 6.5 Energy and sugar content of beverages commonly consumed by children Table 6.6 Genetic disorders associated with early-onset obesity Chapter 07 Table 7.1 Sexual maturation ratings (Tanner stages) Table 7.2 A comparison of nutrient requirements* between adults and children aged 11–18 years Table 7.3 Energy requirements of adolescents are dependent upon physiological development and physical activity level (PAL) Table 7.4 Vegetarian dietary practices Table 7.5 Enhancers and inhibitors of iron absorption Table 7.6 Diagnostic criteria for eating disorders Chapter 08 Table 8.1 General guidelines for intake of sugars, fats and salt by adults Table 8.2 Classifying obesity using body mass index or waist circumference Table 8.3 Global distribution of obesity in adults Table 8.4 World Health Organization diagnostic criteria for the metabolic syndrome Table 8.5 Reference ranges for plasma lipids in adults Table 8.6 Normal and hypertensive blood pressure references Table 8.7 Associations between diet and lifestyle factors and specific cancers Table 8.8 Estimates of risk of cancer associated with high BMI Chapter 09 Table 9.1 Age-related decline in physiological functions Table 9.2 Dietary reference values (United Kingdom) for energy and protein Table 9.3 Causes of anaemia in the elderly population Appendix Table A.1 Common dietary fatty acids Table A.2 The essential and non-essential amino acids Table A.3 The minerals: sources, functions and deficiency symptoms Table A.4 The fat soluble vitamins: sources, functions and deficiency symptoms Table A.5 The water soluble vitamins: sources, functions and deficiency symptoms List of Illustrations Chapter 01 Figure 1.1 The concept of balance The demands for nutrients comprise metabolic and physiological processes that utilize nutrients Supply is determined by intakes of food, availability of nutrient stores and de novo production of nutrients Figure 1.2 The association between nutrition and health The requirements of the body for nutrients will be met by a broad range of intakes Very low and very high intakes of any nutrient will be associated with ill health The transition from intakes that are meeting demands and at which risk of disease is low to intakes that would be associated with disease is not abrupt Figure 1.3 Determining nutrient requirements using the balance method Precise measurements of nutrient intake and of output by all possible routes enable determination of nutrient requirements The highest level of intake at which balance can no longer be maintained will indicate the actual requirement of an individual for that nutrient Figure 1.4 The individual response to food is complex and determined by a range of modifiable and non-modifiable factors Figure 1.5 Single nucleotide polymorphisms (SNPs) arise when there are single base changes in the DNA sequence of a gene As all individuals carry two copies of a gene, the polymorphism can result in individuals being homozygous or heterozygous for specific gene variants Figure 1.6 The CT677 SNP of methylenetetrahydrofolate reductase (MTHFR) influences the activity of the enzyme in tissues This common variant of the gene can have significant impact on folate metabolism Figure 1.7 Body mass index (BMI) is commonly used to define and classify overweight and obesity Figure 1.8 Availability of animal and plant protein by world region Per capita availability of protein from plant and animal sources calculated from the 2004 FAO global food balance sheets Figure 1.9 A food frequency questionnaire is used to estimate the habitual consumption of foodstuffs within the diet of an individual Figure 1.10 The doubly labelled water method is a technique used to assess energy expenditure Subjects consume water containing stable isotopes of hydrogen and oxygen This water reaches equilibrium with the body water Measures of the doubly labelled water in saliva and urine enable estimation of the loss of 18O2 from body water That loss can only occur through production of labelled carbon dioxide Carbon dioxide production is a measure of metabolism Figure 1.11 Measuring the relationship between a nutritional exposure and a disease outcome is complex, necessitating careful epidemiological designs These designs must consider appropriate sampling in terms of size of population, length of study, measurement of diet and measurement of disease outcome Figure 1.12 A confounding factor is an additional factor that may explain the relationship between an exposure and an outcome The confounding factor is related to both outcome and exposure, but does not lie on the causal pathway between the two Figure 1.13 Understanding odds ratios a) Odds ratio (OR) is a descriptor of the risk of event compared to a reference group For the reference, the OR is set at 1.0 If OR is less than 1.0, that indicates decreased risk If more than 1.0, it indicates increased risk b) OR is an estimate of risk and the quality of that estimate will depend upon methodological factors and biological variation The range of possible values for OR is represented by 95% confidence intervals These are used to distinguish between OR estimates that show a significant relationship between exposure and risk and those which do not Figure 1.14 Hierarchy of evidence in nutrition–disease studies Experiments in animals or in vitro have the lowest methodological quality, while randomized controlled trials and meta-analyses are of highest quality Figure 1.15 Research designs in epidemiology Figure 1.16 The association between risk of nutrition-related risk and level of nutrient intake EAR, estimated average requirement; RNI, reference nutrient intake; UL, tolerable upper limit Figure 1.17 The normal distribution as a basis for DRVs UK DRVs are based upon an assumed normal distribution of individuals’ nutrient requirements and level of nutrient intake The estimated average requirement (EAR) is set at the centre (mean) of the distribution The lower reference nutrient intake (LRNI) and reference nutrient intake (RNI) values are placed two standard deviations below and above the mean, respectively The nutrient requirements of all but 5% of the population should therefore be met by levels of intake between these two values Chapter 02 Figure 2.1 Maternal and neonatal mortality a) Maternal mortality declined in most regions of the world between 1980 and 2008, but remains markedly higher in the developing countries b) There is considerable global variation in neonatal mortality, with highest mortality in the African nations (figures shown for 2009–2013 in selected countries) Figure 2.2 The endocrine control of female reproductive function The menstrual cycle lasts for an average of 28 days This can be divided into a distinct follicular phase (days 1–13) during which oestrogen, LH and FSH stimulate follicular development Ovulation driven by high concentrations of LH and oestrogen occurs on day 14 The luteal phase (days 15–28) is driven by hormone production from the corpus luteum, which produces high concentrations of progesterone and oestrogen to prepare the uterine lining for implantation of a fertilized embryo In the absence of fertilization, feedback inhibition of progesterone promotes the degeneration of the corpus luteum and menstrual bleeding Figure 2.3 Polycystic ovary syndrome (PCOS) is alleviated by weight loss Approximately 50% of women with PCOS are overweight and obese PCOS symptoms can be reduced by weight loss, achieved through increased physical activity and dietary change or by treatment with metformin Metformin is an anti-diabetic drug, which acts by suppressing hepatic gluconeogenesis Figure 2.4 Adipose tissue-derived leptin and the hypothalamic–pituitary–ovarian axis Leptin from adipose tissue promotes production of GnRH, FSH and LH and therefore has a stimulatory effect on the hypothalamic–pituitary–ovarian axis Figure 2.5 Leptin receptor signalling cascade Binding of leptin to the membrane bound Ob-Rb receptor activates multiple signalling pathways, including the phosphoinositol 3 kinase (PI3K) pathway and the RAS–MAP kinase pathway Binding of leptin activates JAK2, which phosphorylates STAT3 Formation of phosphorylated STAT3 complexes drives activation of transcription of target genes including NPY and AgRP Leptin resistance develops through leptin up-regulation of the expression of suppressor of the cytokine signalling-3 (SOCS3), which inhibits the JAK2–STAT3 pathway Figure 2.6 ROS are damaging within biological systems a) A section of membrane in a mammalian cell comprises the phospholipid bilayer with a transmembrane protein and cell surface proteins b) After interaction with a reactive oxygen species, the section of membrane is heavily damaged due to the chain reactions established by the oxidation of macromolecules Oxidative damage to the lipid bilayer (lipid peroxidation) will impact upon membrane properties such as permeability Damage to proteins will alter conformation and impact upon receptor, signalling, transport and enzyme functions Figure 2.7 Endocrine control of male reproductive function In males, pulsatile hypothalamic production of GnRH stimulates the release of FSH and LH which stimulate the production of testosterone and the development of mature sperm in the testes Testis-derived inhibin-B and testosterone have negative feedback effects in the anterior pituitary and hypothalamus and thereby regulate the hypothalamic–pituitary– testicular axis Figure 2.8 The formation of mature sperm Sperm production in the male reproductive tract consists of mitotic and meiotic divisions followed by a differentiation phase in which sperm acquire their specialized structures Figure 2.9 Contemporary trends in sperm counts The assertion that sperm counts fell sharply between the 1940s and 1990s has been widely disputed However, data from recent surveys using robust methodologies often indicate a progressive decline over a more recent period Figure 2.10 The relationship between male obesity and subfertility Obesity and insulin resistance are a cause of infertility as they interfere with the normal secretion and transport of androgens As androgens are activators of lipolysis, further adiposity is stimulated by impaired action of the androgens Figure 2.11 The impact of alcohol intake on sperm count is minimal Moderate intake of alcohol is not associated with adverse effects upon sperm counts Hansen et al (2012) compared men consuming 96 units of alcohol or more with non-consumers Martini et al (2004) considered any alcohol consumption against non-consumption, and Joo et al (2012) evaluated the effect of >33 g alcohol/day against