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Human lactation and the structure of infant feeding
Much human behaviour has characteristics that we share with other species among the primates, the order to which Homo sapiens belongs. But we share the way we feed our young much more widely with other species of mammals, the class to which the primates belong. Indeed, the defining characteristic of this class is the feeding of their young on milk, and the class is named for the mammary glands that make this possible. Because infant mammals are initially fed exclusively on milk, it contains a large number of different nutritional constituents. The largest is water. It also contains energy-yielding components, which include a sugar, lactose, and fats, which provide a particularly dense source of energy, and it contains protein, in the form of casein and whey protein. These constituents of milk provide for the initial growth and energy expenditure of infants after birth. A range of immunological constituents help protect the infant against disease.
Feeding their young on milk has been a very successful adaptation for mammals; indeed, Caroline Pond has argued that it has been a major determinant of their ecological role (Pond, 1977; 1983). Although some reptiles guard their young as a form of parental care, reptiles do not bring food to the nest. The young must forage for themselves, and reptiles must therefore reproduce in environments that provide a supply of food suitable for infants as well as for adults.
In previous chapters we have dealt with adverse effects of undernutrition in children. This is a widespread problem of long standing, and in many countries it is one that has been improving in recent years. A more recent problem and one that is clearly getting worse is ‘overnutrition’ – the increased fat storage that results from a higher food intake than is necessary to provide for a child's energy expenditure.
The body of a child can be thought of as comprising different compartments, which may be identified in terms of the tissues involved (for example, bone, muscle, adipose tissue, blood) or in terms of their chemical composition (for example, mineral, protein, fat, water). The two do not correspond exactly. Fats have a wide range of different functions in the body (Pond, 1998). The brain, for example, is about 60% fat, mostly in the form of phospholipids and cholesterol in cell membranes. These are structural lipids. Adipose tissue, which is unique to vertebrates, differs from other fat containing tissues in the body because it has evolved as a specialised store of fat, available to provide energy as required. The fat is stored in the specialised fat storage cells of the body, the adipocytes, which contain storage lipids based on triacylglycerol molecules. It is these storage lipids that we are concerned with here, so measuring adiposity is simple in theory – we dissect out the adipose tissue, extract the storage lipids from it and weigh them.
My aim in this book is to summarise recent research dealing with psychological aspects of nutrition in childhood. Broadly speaking, these psychological aspects involve two kinds of problem – those concerned with the development of behaviour that is related to food intake, and those concerned with the later consequences of malnutrition, or more generally with the later consequences of different types of nutrition. The overall organisation of the book is developmental. I deal in turn with problems that arise before or around the time of birth, with problems associated with infancy and the weaning period, and with problems which are more characteristically associated with later childhood and adolescence. These are the major transitions. Birth is a major transition because although malnutrition can arise before or after birth (and malnutrition in both periods can have effects on the child's development), its causes before and after birth are obviously different: only malnutrition after birth can result from problems with the child's own feeding behaviour, for example. Weaning is a major transition between two quite different kinds of feeding behaviour. Adolescence and the period preceding it involve transitions of a different kind, characterised by changes in the meaning and significance of food and body weight rather than in the nature of eating behaviour and the foods that are eaten. But although the overall organisation of the book is developmental, some departure from this order is necessary, and there cannot, of course, be any strict demarcations between the different stages of life.
There are potentially many types of nutritional deficiency, because food contains many different nutrients. Golden (1995) classifies them into two types. Type 1 nutrients are needed for specific metabolic functions, and deficiencies in these nutrients lead to specific clinical signs that are characteristic of deficiency diseases, such as beri-beri (a result of vitamin B1 or thiamine deficiency), scurvy (vitamin C or ascorbic acid deficiency), xerophthalmia (vitamin A or retinol deficiency). There are body stores of most of the nutrients in this class. When consumption of the nutrients is inadequate, growth continues but the body stores of the nutrient are used up, leading to the specific clinical signs. These deficiencies can be measured biochemically (for example, by measuring thyroxine in iodine deficiency disorders). Type 2 nutrients, on the other hand, are needed for metabolism in general in all the tissues and organs of the body. These include the components of protein, but also, for example, zinc, potassium, sodium and magnesium. There are no body stores of most of these nutrients except the normal tissues of the body. So rather than leading to specific nutritional deficiencies with specific clinical signs, an inadequate intake of any of these nutrients leads to a generalised growth failure. There are no specific biochemical tests for these deficiencies. They are normally detected by the associated growth failure, measured anthropometrically.
The Nutritional Psychology of Childhood is a systematic account of research on the psychological aspects of nutrition in children from birth to adolescence. It deals with two major themes: the development of eating and the effects of malnutrition on the developing child. Robert Drewett discusses the developmental problems that arise with eating and food intake, including nursing and weaning in infancy, the handling of solids and the development of food choice and eating habits. Nutritional problems are considered in children born preterm or small for gestational age, or whose growth is poor, in children who are iron deficient or more generally malnourished, and in children with physical illnesses, including phenylketonuria and cerebral palsy. The development of eating disorders and obesity are also considered. Drawing on research from both developing and industrialised countries, this book will be of interest to students, researchers and professionals in psychology, nutrition and child health.
Weaning and the development of independent eating skills
Because of their early dependence on the mother's lactation, the development of feeding behaviour in mammals involves a striking discontinuity at the time of weaning. Weaning involves three separate changes, though they are linked in time. Firstly, there is a change in the kind of food taken, from milk to a range of solid foods. Secondly, there is a change in the mechanics of feeding behaviour, from the sucking characteristic of an infant feeding on milk to the biting and chewing characteristic of older children and adults feeding on solid foods. This change in the mechanics of feeding behaviour is only partly linked to changes in the kind of food taken. Adults, for example, also drink milk, but they do not drink it in the way infants do. Thirdly, there is a change from an obligatory dependence on the mother or another carer to more independent feeding. Because the diet of adults involves a wide range of foods, weaning calls for an extensive learning process, in which a child comes to distinguish foods from things that are not foods, and to choose between different foods.
As we saw in Chapter 1, the average energy expenditure of infants increases steadily over the course of the first year, from about 1 MJ per day at 1 month to about 2.5 MJ a day at 8 months, an increase of 150%.
Criteria for failure to thrive and its epidemiology
In the UK and many other countries infants are weighed at intervals through the first year of life. Figure 7.1 shows the weights of an infant recorded in the first year and plotted on a chart. The lines on the chart are intended to represent the distribution of weights of infants in the UK as a whole over the first year of life. Because the distribution differs in boys and girls, boys and girls have different charts. This was a boy. At birth his weight lay almost exactly on the 50th centile, i.e. it was very close to the average for British boys. But his weight gain over the first year was very slow. By 6 weeks he was below the 2nd centile. Only one or two boys in 100 would weigh less. By a year he was on the 0.4th centile. Only three or four in 1000 would weigh less.
If this were your child, you would probably be worried. Certainly your health visitor would be. But what is there, exactly, to be worried about? One possibility is that the child is ill. Poor weight gain in infancy can be a sign of a previously undetected physical illness – of cystic fibrosis, for example. Often, however, it is not, at least in societies in which health and health care are generally good. But if the child is not ill, poor weight gain is usually due to inadequate food intake.
A woman in Madrid called the emergency services because her child wasn't eating his yoghurt (Corral, 2004). A father suffered a panic attack after accidentally giving his 11-month-old daughter a fruit smoothie that contained a tiny proportion of honey (Wilson, 2005). I dare say these are extreme cases, but parents do seem to show a remarkable degree of anxiety over the feeding and nutrition of their children, and not only parents. According to one recent report, poor nutrition may cause dyslexia, dyspraxia, autism, learning difficulties, irritability, anxiety, lethargy, insomnia, tiredness, depression, anti-social behaviour, reduced sense of smell and taste, cravings, mood swings, hyperactivity, poor concentration and tantrums (Purvis, 2005).
If only one thing is clear from this book, I hope it will be clear quite how difficult a task it would be to investigate all these possibilities. Effects of the principal known nutritional deficiencies on intellectual development in children have been of interest for at least 50 years, but it is very hard to be certain even of the significance of these. Iron deficiency is measurable and much of the biochemistry of iron is quite well understood. There are large numbers of iron-deficient children, and the prevention and treatment of iron deficiency is possible in principle, using procedures that are cheap and relatively safe, and can be implemented in double-blind trials so that investigators can test the children without knowing whether they have been given iron supplements or not.
Feeding, like breathing, is central to our survival. I do not mean to the survival of ‘our species’ but literally to the survival of each one of us. Yet, unlike breathing, it has never been very clear to what discipline the study of feeding belongs. In respect of children it is the province of midwives and health visitors, of paediatricians and specialist nurses, of speech therapists, of dieticians and nutritionists, of child psychiatrists, of psychologists, and of others, no doubt, as well. To some extent this may reflect the rather uncertain academic position of the study of nutrition more generally. Whatever the reason, published research concerning psychological aspects of nutrition in childhood is very widely scattered, and this is, I believe, the first attempt that has been made by a single author to gather it together in one place in the form of a book. No doubt the attempt will leave a lot to be desired, but I hope that it will provide at least an initial source and a reasonably useful framework for those who need them in first approaching this area.
Tastes will differ, but speaking for myself I do not enjoy reading reviews that report findings without giving any indication of the nature or quality of the research that gave rise to them, so I have tried to say enough about the research I cite at least to give a flavour of the methodology used in it.
In infancy and early childhood there are three ‘feeding and eating disorders’ that are formally recognised in DSM-IV, the Diagnostic and Statistical Manual of Mental Disorders of the American Psychiatric Association (APA, 1994). The first two are pica (the persistent eating of non-nutritive substances) and rumination disorder (the persistent regurgitation and rechewing of food). Both these are often associated with developmental disabilities. The third, feeding disorder of infancy or early childhood, essentially refers to failure to thrive when it is associated with failure to eat adequately.
The eating disorders that characteristically arise over the period around puberty, however, are much more obviously psychiatric disorders, related to depression and the other affective disorders of adults. In DSM-IV two eating disorders are given specific diagnoses, anorexia nervosa and bulimia nervosa. A third category, eating disorder not otherwise specified, is used when some of the criteria for the two specific diagnoses are met, but not others.
There are four diagnostic criteria for anorexia nervosa (APA, 1994). The first involves a refusal to maintain a body weight at or above a defined minimum, specified as 85% of the ‘expected’ weight given the person's age and height. This may result from a loss of weight, or in young people who are still growing, from a failure to gain weight. The second is an intense fear of gaining weight or becoming fat.
Nutritional deficiencies in childhood tend to be most prevalent in the first three years. This is partly because young children have relatively high nutritional needs. They are growing rapidly in the years immediately after birth, and their small body mass gives them a relatively higher requirement for energy, as they lose heat more readily. In addition, as noted at the end of Chapter 3, in many countries there is a high prevalence of infectious disease in the early years, with diarrhoeal disease, particularly, leading both to anorexia and reduced food intake, and to poorer absorption of the food that is eaten. And the weaning of infants in the first year calls upon them to learn a whole new range of feeding skills which are initially not well developed.
Up to the time of birth, of course, an infant's nutrition is derived entirely from the mother, via the placental circulation. But this does not mean that all children receive the optimal nutrition before birth, or that malnutrition cannot occur before birth. It can and does. In considering the effects of malnutrition on psychological development, therefore, we need to begin at the earliest stages of development and consider first effects that might result from malnutrition occurring in the first nine months from conception, when the child is usually still in utero.
At the end of Chapter 3 we considered the effects of diarrhoeal diseases on food intake and growth. Diarrhoeal diseases are usually temporary, and can affect any child. In this chapter we will consider nutritional problems associated with some long-term illnesses or disabilities. Almost all long-term illnesses and disabilities have nutritional aspects to them and the examples considered here are just examples. I have chosen these examples because they illustrate important general principles (PKU), because nutritional aspects are central to the disorder (cystic fibrosis), because there can be a tendency to overlook disorders that are found only in minority ethnic groups (sickle cell disease) or because they relate to other problems dealt with in other chapters (cerebral palsy). But mainly I have chosen them because interesting and important research is available on them.
Phenylketonuria (PKU) has been described as a classic example of a genetic disorder (Scriver & Clow, 1980a; 1980b). It is inherited as an autosomal recessive trait. As a recessive trait, PKU develops in the child only if they have two copies of a gene for the condition. If both parents are heterozygotes (i.e. if they each have a single copy of the gene) one in four of their children, on average, will have two copies and so will develop the disorder. Children with a single copy are carriers, and they are only slightly different from children without any PKU genes.
Feeding behaviour in the weaning period is important theoretically and practically. The aim of the study was to develop appropriate observational codes for its description, to assess their reliability, and to examine the relationships between feeding behaviour, meal duration, and food intake. One hundred children aged 12–14 months were visited in their own homes, and two of each child's usual meals video-recorded and analysed using direct observation. Codes were developed that distinguished between the mother feeding her child directly and assisting her child's self-feeding, and between the child's behaviour when responding to being fed by the mother and when feeding themselves. All-occurrence sampling was used to record counts of these feeding acts during the meals. Two observers replicated coding of 40 randomly chosen meals to determine the reliability of these counts. Except for three codes which were used very infrequently (median counts of zero over the 200 meals), reliability was high with ρ > ·80. There was wide variation in the extent to which individual children fed themselves during meals, with only moderate consistency from meal to meal. Food intake was uncorrelated with meal duration, but correlated with the number of bites of food taken. Adjusted for the number of bites, longer meals were associated with a lower intake. When fed by the mother the child's food intake was greater than when they fed themselves, but the duration of the meals was little affected. The coding scheme is simple to use and generally reliable, and provides a means for relating more global measures of emotional or other characteristics of mealtime behaviour to feeding behaviour and nutritional intake.
To examine the possibility that there is an early sensitive period for the effects of malnutrition on cognitive development, three groups of children (N = 197) were recruited from a birth cohort with known growth characteristics in south-west Ethiopia (N = 1563). All had initial weights [ges ]2500g. Early growth falterers dropped in weight below the third centile (z<−1·88) of the NCHS/WHO reference population in the first 4 months. Late growth falterers were children not in the first group whose weights were below the third centile at 10 and 12 months. Controls were a stratified random sample with weights above the third centile throughout the first year. All children were tested blind at 2 years using the Bayley Scales of Infant Development, adapted for use in Ethiopia. Mean (SD) scores on the psychomotor scale were 10·2 (3·7) in the controls, 6·6(4·2) in the early growth falterers, and 8·5(4·3) in the late growth falterers. For the mental scale they were 28·9(5·8), 22·6(6·2), and 26·6(6·1) respectively. Both overall differences were statistically significant at p<·001, and planned comparisons between the control and the combined growth faltering groups, and between the early and later growth faltering groups, showed that each difference was statistically significant for both scales. However, early weight faltering was associated with weight at the time of testing (r = .33), which was associated with scores both on the psychomotor (r = .53) and the mental scale (r = .49). After taking weight at the time of testing into account there was no additional effect attributable to the timing of growth faltering. In this population, therefore, early malnutrition does not have specific adverse effect beyond the contribution that it makes to enduring malnutrition over the first 2 years.