FIGURE 7-2 The energy cost of growth. (A) Cost calculated from lean and fat gains derived from the body composition data of Fomon SJ, Haschke F, Zeigler EE, Nelson SE. Body composition of reference children from birth to age 10 years. Amer J Clin Nutrit. 1982;35:1169-1175; and Guo S, Chumlea WC, Roche AF, Siervogel RM. Age- and maturity-related changes in body composition during adolescence into adulthood: The Fels Longitudinal Study. Int J Obes. 1997;21:1167-1175, and assuming an energy of fat-free mass and fat of 1.6 and 9.3 Kcal/g and an energy cost of synthesis of 15%; ♦—♦ Boys, ■—■ Girls. (B) The energy cost of growth compared to the U.S. 1989 recommended daily allowance for energy; ♦—♦ Boys, ■—■ Girls, A—A RDA Boys, x—x RDA Girls.
Protein-energy malnutrition (PEM) is the most common and important nutritional deficiency. Half the world's children are said to suffer undernutrition, mainly as protein-energy malnutrition. In its severe form, it exists as kwashiorkor and marasmus. In many African and Asian countries, 1-3% of children under 5 years old suffer severe malnutrition. In its less severe form, it appears as stunting and wasting, depending on the severity and duration of the insult. In developing countries, 10-50% of children are stunted, that is with heights more than 2 SD below reference data medians. The model of malnutrition in developing countries is of an iceberg. For every 1 case of severe malnutrition that is visible at clinics or in hospitals, there may be 15-25 moderate cases and a further 25-35 mild cases in the community. In global terms, the numbers affected may be 150 million.
According to conventional methods of classifying causes of death, malnutrition does not appear a major cause in developing countries and, consequently, receives less of the donor and national health resources. However, results from eight prospective studies in different parts of the world indicate that 42-57% of all deaths of 6- to 59-month-old children are due to malnutrition's potentiating effects on infectious disease. The relative risk of death for severe malnutrition is eightfold, for moderate fivefold and for mild two and a half times that of normally nourished children. However, more than three quarters of the nutrition-influenced deaths are attributable to mild-moderate malnutrition.
We are presented routinely with pictures of malnutrition arising from natural disasters, and it is easy to accept the myth that malnutrition results from scarcity of food. The vast majority of cases of malnutrition have roots more in economic and political considerations, many of which exacerbate any climatic or biological effects. According to the Nobel Prize-winning development economist Amartya Sen, famine has never occurred in a democracy. Inequitable distribution of resources and gender discrimination make a large contribution to malnutrition. It is estimated that 80% of undernourished children live in countries with food surpluses. Suffice to say that malnutrition rarely has its origins in a shortage of food. If we can nourish people at the poles, in the ocean depths, and in space, where no human foodstuffs grow naturally, we have the ability to nourish people in less extreme habitats.
The underlying causes of malnutrition are many, and their interrelationships are complex and diverse. There is a well-documented synergism between nutrition and infection in their effects on growth. The undernourished child is more susceptible to infection and the ill child has higher nutritional requirements at a time when they are likely to be anorexic. The interrelationships are too complicated and context specific to allow this synergism to be easily quantified. Effects on the gastrointestinal mucosa causing malabsorption may predominate. Estimates suggest that perhaps one third of linear growth failure can be ascribed to illness. However, children in rural areas of developing countries who have avoided infection to any significant extent are still 10-15 cm less than American children at 7 years old.
Undernutrition is not a problem confined to developing or transitional societies, to civil unrest and warfare. Poverty, relative and absolute, is found in all countries. Within the United Kingdom, a member of the G7 Group of Industrialized Nations, mortality and socioeconomic differentials have widened over the last 15-20 years and adverse socioeconomic circumstances in childhood influence subsequent mortality that is independent of the continuation of the disadvantage throughout life. From the other end of the social spectrum, affluent parents with particular beliefs about food habits have caused growth retardation in their children.
Studies have been performed on the growth of children consuming macrobiotic diets in Holland, following observations that these children were lighter and shorter than a control group on an omnivorous diet.7 Macrobiotic diets resemble those of many children in developing countries in being based on grain cereals, mainly rice, vegetables, and pulses, foods high in fiber and starch but relatively low in protein and with intakes of calcium and vitamin D substantially below Dutch RDAs. Deviations in growth began in the weaning period with partial catch-up between 2 and 4 years old in weight and arm circumference but not in height. Linear growth was associated with protein content but not energy content of the diet. The children of families that subsequently increased their consumption of fatty fish or diary products grew more rapidly in height than the other children.
These observations are significant as they illustrate that growth is nutrition sensitive even in a good environment. Much of the material concerning developing countries that follows may leave the impression that improving nutrition is not very influential, but this is because those environments contain a number of other impediments to growth.
A key question in human biology over recent years, and one that has received much attention, is to what extent can a growth-retarded child catch up. Martorell, Kettel Khan, and Schroeder hold that stunting (low height for age) arises from events early in life, and once present, it remains for life.8 The contrary view of Tanner is that the undernourished child slows down and waits for better times.9 Tanner considers that, "in a world where nutrition is never assured, any species unable to regulate its growth in this way would long since have been eliminated." Obviously, if a child remains in the environment that led to stunting, it is unlikely that this will be conducive to improvements in growth. However, Adair recently described catch-up between 2 and 12 years of age in Filipino children staying in the same environment.10 Severe stunting in the first 2 years was associated with low birth weight, which significantly reduced the likelihood of later catch-up. Positive attributes associated with catch-up were taller mothers, being the first born, and fewer siblings, which illustrates again the actions of intervening nonnutritional factors.
There is a remarkable feature in the growth of children in India, the Gambia, West Africa, and elsewhere who were stunted, in some cases severely stunted, before 5 years old and remain stunted at 18 years old. The growth increment between 5 and 18 years may match that of western children.11 The growth pattern is not the same, as puberty is later and prolonged. It is not clear how this comes about. It is almost as though the last chance for catch-up is taken. Perhaps, growth in height is replaced by another factor, growth in weight or physical activity, in the front line of impairments.
In contrast to height deficits, weight deficits increase from childhood to adulthood in almost all populations with childhood growth retardation. This may have significant and long-lasting consequences as weight for age and weight for height may be more important than height per se in terms of functional outcomes such as work capacity, earning power, and employment. Linear growth has tended to receive more attention by auxologists than growth in mass, but this bias decreased in recent years.
Improvements in the environment result in catch-up growth, but such improvements are not common. Reports of the long-term effects of treating children with malnutrition provide evidence of catch-up, even though treatment may be for only a short period and the child returns to the same environment. Community-based supplementation studies provide better evidence of what can be achieved in the habitual environment, as described next. Any prediction as to whether catch-up growth will occur in an individual or population requires a full environmental assessment.
Relocation to better environments in the form of migration or adoption involves changes in the environment not restricted to nutrition. Studies of refugees and adoptees from South and Southeast Asia have shown accelerated growth rates, but it is not yet clear if these translate to increased adult stature. There is some evidence of accelerated puberty, which may have the effect of shortening the growth period and curtailing adult stature.
Supplementation is taken to be an addition to a diet to make up all or part of a deficiency. It can vary according to the type, amount, and duration; hence, a dose-response effect should be observed. Thus, it is a classical research design of high internal validity to demonstrate the presence of undernutrition and its effects on growth. This is also a common approach to improving maternal and child health. It might be thought that supplementing the diet of children and mothers in populations with low growth rate would inevitably result in improved growth. However, when this is attempted, the effects are usually much smaller than expected, and growth never achieves the levels of the most affluent groups in the same population or the median values in western reference data.
Several extensive supplementation studies are described in the literature. One such is the Institute of Nutrition of Central America and Panama (INCAP) longitudinal study of the effects of chronic malnutrition on growth and behavioral devel opment that began in 1969. It is unusual, in having a follow-up component several years after supplementation ended.12 The study was conducted in four villages, which began with small and light mothers on low dietary intakes and with weight gains in pregnancy half those of well-nourished women; 15% of the infants died in the first year of life. Two types of supplement were provided to children up to 7 years old. Two villages selected at random were provided with atole, a protein-energy supplement, and the other two with fresco, a no-protein supplement with one third the energy content of atole. Both supplements contained minerals and vitamins, and preventative and curative medicine were provided to all villages. Supplement take-up was voluntary and so varied widely, but this allowed a dose-response approach to the analyses using multiple regression and for confounding factors to be taken into account.
Birth weights increased, but only by some 7 g per 10 MJ of supplement. However, low birth weight and infant mortality fell by a half in those with high supplement intakes. Energy intake was more important than protein for these improvements. In 0- to 3-year-old children, greater supplementation was associated with better growth in supine length and weight but not limb circumferences or skinfold thicknesses. In the highest supplementation group, these differences were 1 kg and 4 cm at 3 years old. Supplementation of 420 kJ (100 kcal) per day was associated with additional length gains of 9 mm in the first year, and 5 and 4 mm in years 2 and 3, but had no effect after 3 years of age. Children from supplemented villages continued to weigh more, be taller, and to have higher lean mass at adolescence, although differences in height were reduced compared to those at 3 years old. Other studies have been analyzed differently but show similar finding when an age-stratified approach is used. Therefore, the effects of supplementation are small and less than expected. The supplemented children did not approach the levels of height and weight seen in more affluent groups or in some other developing countries; and as only some 15% of the energy of the supplement is utilized in growth processes, the fate of most of the supplement is not clear. These data come from research studies that are likely to be more successful than feeding programs because of the enthusiasm of the workers.
There are several possible explanations for this.13 It may be the result of poorly designed and implemented feeding programs. Alternatively, it may be that the hypotheses and models of the processes involved have been unduly simplistic and inappropriate. The supplement may not reach the intended recipient or it substitutes for rather than supplements the habitual diet. "Leakage" and substitution should not be seen as failures of supplementation, as they may have benefits, albeit away from the intended recipient. The supplement may lead to increased activity, with the benefits of play and fitness and social competence, rather than growth.
Lindsay Allen, in her exemplary review of nutritional influences on linear growth, concluded that there was a lack of clear, consistent evidence and that supplementation of zinc, iron, copper, iodine, vitamin A, or indeed energy or protein alone benefited linear growth in growth faltering in developed countries.14 In some studies, improvements were seen; in others, weight gain alone was affected; and in still others, there was no effect whatsoever. However, most of these studies have been on children older than the age at which growth faltering is most rapid. Alternatively, multiple deficiencies may be the cause of growth faltering. Except in the case of iodine, low energy diets are usually low food diets, which means low nutrient diets; that is, multiple nutrient deficiencies.
Growth retardation due to zinc deficiency was first described in the Middle East in the 1960s. Zinc deficiency was associated with high fiber, low protein diets and with parasitic infections. High-level supplementation of zinc was necessary to achieve improvements in growth presumably because the high phytate content of the high fiber diets reduced its bioavailability. Supplemental zinc has been given to low height-for-age well-nourished children in developed countries with variable effects. Linear growth is often improved but not weight gain. Often, there is no reason for these children to be zinc deficient unless they have unusually high dietary requirements for zinc. The role of zinc in the linear growth retardation of developed countries requires further work.
The most widespread dietary deficiency in North America is of iron. The incidence of childhood anemia has been falling at a time when iron-fortified formulas and cereals have become widespread and supplemental food programs have been introduced. Linear growth usually improves in response to iron treatment in anemic children. Iron deficiency also has nonhematological effects.
Nonnutritional factors, such as the social, economic, and biological environments, are important in determining the response to supplementation. In each community, different factors may operate, and there may be no circumventing the need for a full description of the ecology of the community. Our hypotheses and our models and methods of analyses may need to be refined to identify better what needs to be measured. There are, however, limits to the number of variables that can be studied, determined by the cost and quality of the data obtained. However, these studies provide good examples of the fact that diet does not operate in isolation but in concert with other environmental challenges, such as disease, poor schooling, and general deprivation. (Some of these issues are described in Chapter 8, "Environmental Effects on Growth," and Chapter 9, "Social and Economic Influences on Growth and Secular Trends.") The answer would then seem to lie in general environmental enrichment. But, in the absence of endless resources, the key deprivations in each particular case need to be established by ecological study and a more targeted approach to entitlement, enrichment, and empowerment adopted.
Malnutrition in the form of overnutrition or obesity is a major nutritional problem in the western world and is becoming common in other parts, too. Here, too, the obvious assumption, that obesity has its origins in gluttony and that the appropriate remedial action is to reduce dietary intake, may not be valid. Obesity can arise only through a positive energy balance, but this does not need a high energy intake to develop. Low levels of physical activity, inactivity with roots in car use and leisure time TV viewing or computer and games console use, is a major eti-ological factor. Any lowering of energy intake in such children would have an increased risk of precipitating nutrient deficiencies, although changes in the types of macronutrients consumed, such as less fat and a lower energy-dense diet, may be beneficial. Rather, the negative energy balance should be brought about in the main by increased physical activity. From this will flow all the other major health benefits associated with increased activity, fitness, and altered body composition, including increased self-esteem. However, the difficulty of achieving and maintaining weight loss should not be underestimated but should be used as a motivation for avoiding overweight and obesity.
One problem in the area of childhood obesity is how to define it. In adults, we have imperfect but widely accepted indices, such as body mass index and waist circumference, for which particular values or cutoffs have been associated with a variety of risk factors, of morbidity and mortality. It then is possible to specify "healthy" or "recommended" levels. In children, the median value and other per-centiles vary with age and not always in a linear or predictable way; and as yet, few studies have linked these indices to risk factors and very few with outcomes such as morbidity and mortality. Because of this, obesity may then be defined on a statistical basis, such as BMI above the 85 percentile, which is not entirely satisfactory. (See Chapters 16 and 18 on "The Assessment of Human Growth" and "Growth References and Standards.") Bearing in mind the difficulties in assessing the global prevalence of obesity in children and adolescents because of the differing indices employed, longitudinal studies suggest it has doubled in the last 20 years. The measurement and long-term health risks of childhood and adolescent fatness have been well reviewed recently.15
The extent to which obesity in childhood persists into adulthood seems to depend on the time interval between the occurrence in childhood and adulthood. Thus, obesity in adolescence seems more persistent than obesity in childhood. This is the "recency" effect. Until now, most obese adults were not obese as children, but as the prevalence rises, this finding may change.
transitions in nutrition and growth
It is unlikely that humans would have evolved so successfully if they had selected inappropriate diet types. However, it is equally true that the rate of adoption of new and manufactured foods (decades) is much greater than the rate of human evolution (tens of generations), and we cannot assume that we are well adapted to contemporary foodstuffs and diet types. Some 50% of dietary energy in the world is from cereals or cereal products, but only in evolutionarily recent times has this become the case. The domestication of plants and of animals, begun 10,000 b.p., that is, 500 generations ago, altered the diets of humans more than any previous subsistence change. Our societies and cultures have changed, too, and in ways such that technology and globalization have not been uniformly beneficial. Therefore, nutritional problems, albeit different problems to those of the distant past, exist in conditions of affluence.
Nutrition is usually ascribed a key role in the improvements in growth in Europe and other parts of the world over the last centuries. The evidence for this is much less extensive and definitive than we would like, and improvements in growth would not have occurred without concomitant improvements in housing, sanitation, and health provision. (Secular trends in growth are discussed in Chapter 9 on "Social and Economic Influences on Growth and Secular Trends.") How these transitions will continue in the future and what new ones will appear in the short or long term is in the realm of prediction but something for which the students of today may have the answer in their lifetime. A major epidemiological interest of the present centers on the hypothesis that maternal and fetal undernutrition program the body to respond to subsequent affluent nutrition in ways that lead to a number of degenerative diseases. If true and if mothers and fetuses are no longer exposed to under-nutrition in developed countries, then we may see a reduction in the incidence and mortality from these degenerative diseases, as is happening already in much of the developed world. However, much of the rest of the world has yet to experience the first stage of this transition. In many parts of Africa, some of which have a host of other health problems such as the prevalence of HIV infection, nutritional health seems set to fall, at least in the short term. This will have an impact on the growth of the next generation of children.
annotated bibliography Nutrition Textbooks
There is no shortage of choice of nutrition textbooks for U.S. students. I am not familiar enough with all of them in their most recent editions to be able to identify one or two for specific mention. Most are very student friendly, well written and illustrated, with good structure and development of material, end of chapter summaries, assessment activities, and nowadays, lists of Web-based resources. There is some variation in the amount of basic biochemistry and anatomy and physiology that is included. Two examples on my shelf are G. M. Wardlaw and P. M. Insel's Perspectives in Nutrition (St. Louis: Mosby, 1993) and E. N. Whitney and S. R. Rolfes' Understanding Nutrition (Minneapolis: West Publishing Co., 1996). One disadvantage of these types of books is that they are written at length, typically more than 500 pages, and in detail, although not necessarily in great depth, for students of nutrition.
Barasi ME. Human Nutrition; A Health Perspective. London: Edward Arnold, 1997. This book is recommended for any student with no background in nutri tion but taking it as part of a wider program. It is well-written and tackles the fundamental issues clearly and concisely. There is little on Third World issues.
Gibson RS. Principles of Nutritional Status Assessment. New York: Oxford University Press, 1990. The word principles in the title of this book belies the detail and scope of its contents (691 pp.). It is a reference book par excellence, well written and with copious appendices of anthropometric and other reference data. It covers the dietary, anthropometric, and biochemical approaches to nutritional status assessment and has a short section on clinical assessment. Its publication was more than 10 years ago, and inevitably, some sections, such as that on body mass index, need updating. The emphasis is more on hospital and laboratory assessment than field surveys in the Third World. In the latter context, more consideration of environmental and ecological factors is warranted.
Mann J, Truswell AS. Essentials of Human Nutrition. Oxford: Oxford University Press, 1998. This book sets out to meet the needs of clinicians, health professionals, and teachers and, according to the publishers, is proving to be very successful. However, it, too, is over 600 pages. Some of the individual chapters can be strongly recommended. Rosalind Gibson's "Dietary Assessment" and "Determining Nutritional Status" covers the material of her book, described later, in a less detailed manner. Stewart Truswell's "Nutritional Recommendations for the General Population" is a tour de force historical and comparative account of dietary recommendations and guidelines. It includes answers to most questions on the principles of establishing recommendations. Better chapters on childhood and adolescence and protein-energy malnutrition are found elsewhere. The standard works on protein-energy malnutrition include J. C. Waterlow's Protein Energy Malnutrition (London: Edward Arnold, 1992).
Webb GP. Nutrition: A Health Promotion Approach, 2nd ed. London: Arnold, 2002. This book is recommended for students of human biology because it treats well the methods of nutritional surveillance and research and, in particular, the types and strengths of evidence. There is little on Third World issues.
A good bookmark for nutrition links is http://www.nutsoc.org.uk/links.htm.
Nutrition topics at the National Library of Medicine are at http://www.nlm. nih.gov/medlineplus/foodnutritionandmetabolism.html.
Nutrition and Growth in Bioanthropology, Growth, and Human Biology Texts
Bogin B. Patterns of Human Growth, 2nd ed. Cambridge: Cambridge University Press, 1999:268-282. The biocultural approach to growth and nutrition by this informed and readable author ensures that the relationships of nutrition and growth are considered within the context of the wider environment.
However, it would be easy to gain the idea from the section on "the milk hypothesis" that there is something specific to milk and its effects on growth of undernourished children not shared by other good sources of nutrients. In practice, its advantages are likely to be in nonnutritional terms such as cost and availability.
Eveleth PB, Tanner JM. Worldwide Variation in Human Growth, 2nd ed. Cambridge: Cambridge University Press, 1990:191-198, 219-223. This is a succinct description of nutrition and growth in infancy and adolescence located in a classical account of environmental influences in growth.
Tanner JM. Foetus into Man, 2nd ed. Ware, UK: Castlemead Publications, 1989:129-140. There is a short informative account of the effects of nutrition on growth and the tempo of growth which is a useful introduction to the topic. The section on experimental models is unusual in such accounts but illustrates well what can be learnt from laboratory-based studies.
Ulijaszek SJ, Strickland SS. Nutritional Anthropology: Prospects and Perspectives. London: Smith-Gordon, 1993:119-131. There is a short section on nutrition and growth but much else of interest and relevance throughout the book, including the consequences of small size, seasonality, and growth and transitions in subsistence.
Ulijaszek SJ, Johnston FE, Preece MA. The Cambridge Encyclopedia of Human Growth and Development. Cambridge: Cambridge University Press, 1998. Many entries are relevant to nutrition and growth in the sections on infant feeding and growth (pp. 320-325), nutrition (pp. 325-333), and elsewhere. These provide useful introductions to a number of topics under these headings. There are extensive lists of up-to-date references.
Zerfas AJ, Jelliffe DB, Jelliffe EFP. Epidemiology and nutrition. In: Falkner F, Tanner JM (eds). Human Growth: A Comprehensive Treatise, 2nd ed. Vol. 2, Postnatal Growth. New York, London: Plenum, 1986:475-500. Although much new data has been collected since this chapter was published, its content and structure, with emphases on methods and approaches to the effects of protein-energy malnutrition on human growth, are exemplary and a valuable source of guidance. The three-volume series is widely available and repays consultation.
Research Reports and Reviews, Including Individual Chapters
The International Dietary Energy Consultative Group (IDECG) produced several research reviews arising from workshops that have the advantage of being available without charge from IDECG or at the United Nations University Web pages (http://www.unu.edu/unupress/food/foodnutrition.html) or as supplements to widely available journals. They are included in this list because of their availability and because they have several papers in each report relevant to this chapter. They are also written by experts in the field and well done. IDECG reports are available from IDECG Secretariat, c/o Nestle Foundation, P.O. Box 581, 1001 Lausanne, Switzerland. (Note: It might be better if lecturers obtained copies from IDECG and placed them in libraries rather than each individual student requesting copies.)
Allen LH. Malnutrition and human function: A comparison of conclusions from the INCAP and nutrition CRSP studies. J Nutrit. 1995;125(Suppl 4):1119S-1126S or Martorell and Scrimshaw IDECG report. This article reviews the evidence that growth stunting occurs early in life and is accompanied by functional impairments. The CRSP studies in Kenya, Egypt, and Mexico suggest poor growth is associated with multiple micronutrient deficiences and have been influential in diverting attention from protein-energy malnutrition to other nutrient deficiences. This was not investigated in the INCAP studies whose children were much more malnourished and stunted.
Allen LH. Nutritional influences on linear growth: A general review. Euro J Clin Nutrit. 1994;48(Suppl 1):S75-S89 or Waterlow and Schurch IDECG report. The paper reviews what is known about the effects of specific nutrient deficiencies on growth faltering. There is no clear, consistent evidence that supplementation benefits linear growth. This may be because the children studied have been beyond the age when growth faltering is most rapid.
Assessment of childhood and adolescent obesity. Amer J Clin Nutrit. 1999; 70(Suppl 1):123S-173S. Considerations of height, weight, and body mass index dominate this recent collection of papers. Visceral fat is discussed by Goran and Bower in relation to disease risk in children and adolescents.
De Onis M, Villar J, Gulmezoglu M. Nutritional interventions to prevent intrauterine growth retardation: Evidence from randomised control trials Euro J Clin Nutrit. 1998;52(Suppl 1):S83-S93 or in the Scrimshaw and Schurch IDECG report. At present, no effective nutritional interventions have been demonstrated to reduce the risk of intrauterine growth retardation with the possible exception of balanced protein-energy supplementation. The authors emphasize the gap between the size of the problem and the quantity and quality of the data. Further work is necessary on zinc, folate, and magnesium with larger samples.
Golden MHN. Is catch-up possible for stunted malnourished children? Euro J Clin Nutrit. 1994;48(Suppl 1):S58-S71 or Waterlow and Schurch IDECG report.
Himes JH, Story M (eds). Assessment of childhood and adolescent obesity. Inter J Obes. 1999;23(Suppl 2):S1-S58-S64. The expected issues of identification, prevalence, risks, physical activity, prevention, and treatment are covered mainly with a North American perspective. The complexity of the etiology of obesity is described by a new model for treating childhood obesity.
Leon DA. Fetal growth and adult disease. Euro J Clin Nutrit. 1998;52(Suppl 1):S72-S82 or in the Scrimshaw and Schurch IDECG report. This paper is said to put the work of Barker and colleagues into the realm of hypothesis generation as opposed to hypothesis testing. This is because of the use of a retrospective approach to an issue with multiple causes. The conclusion of this thoughtful, well-written paper is that, "At the present time the foetal origins hypothesis should be regarded as an area for basic bio-medical research. It is difficult at this stage to draw strong public health conclusions with the limited state of knowledge."
Martorell R, Kettel Khan L, Schroeder DG. Reversibility of stunting: Epi-demiological findings in children from developing countries. Euro J Clin Nutrit. 1994;48(Suppl 1):S45-S57 or Waterlow and Schurch IDECG report.
Martorell R, Scrimshaw NS. The effects of improved nutrition in early childhood: The Institute of Nutrition of Central America and Panama (INCAP) Follow-up Study. Available as J Nutrit. 1995;125(Suppl 4):1027S-1138S or as an IDECG report. The INCAP study and its follow-up are the first comprehensive long-term evaluation of a nutrition intervention aimed at mothers and children in a developing country. These peer-reviewed papers might normally have been published individually in a variety of journals and it is a great service to the student that they appear in one volume.
Norgan NG. Chronic energy deficiency and the effects of energy supplementation. In: Schurch B, Scrimshaw NS (eds). Chronic Energy Deficiency; Consequences and Related Issues. Lausanne: IDECG, 1987. This paper reviews the effects of dietary supplementation in chronic undernutrition and considers why supplementation has small effects. It identifies the need to move from simple main effects models to studies of the indirect multistage processes involved and the indirect effects on the family.
Schurch B, Scrimshaw NS. Chronic Energy Deficiency; Consequences and Related Issues. Lausanne: IDECG, 1987. The first IDECG report summarized knowledge on how chronic energy deficiency can affect pregnancy, lactation, and childhood; work capacity and performance; and social and economic development.
Scrimshaw NS, Schurch B. Causes and consequences of intrauterine growth retardation. Available as a Euro J Clin Nutrit. 1998;52(Suppl 1):S1-S103 or as an IDECG report. This is a timely report, given the importance now being attached to early nutrition reducing infant and childhood malnutrition and the hypothesis of effects arising in adulthood. It includes a systematic review of 126 randomized control trials with 36 kinds of interventions.
Waterlow JC, Schurch B. Causes and mechanisms of linear growth retardation. Available as Euro J Clin Nutrit. 1994;48(Suppl 1):S1-S216 or as an IDECG report. Much is known about the epidemiology and natural history of stunting. Much less is known about the actual causes and mechanisms. There is epidemiology here, too. The papers on catch-up growth by Martorell, Ket-tel Khan, and Schroeder and by Golden should appear in any reading list on the topic.
The home page of the International Obesity Task Force with a section on childhood obesity and links to other obesity sites is at http://www.iotf.orgV.
These have been included in the text to support or as sources of statements. Not all are annotated, rather their significance is indicated by their context.
1. FAO, WHO, UNU. Energy and Protein Requirements. Technical Report Series No. 724. Geneva: World Health Organization, 1985. Useful as a source of information on the methods adopted to set protein and energy requirements internationally and those requirements.
2. Department of Health. Dietary Reference Values for Food Energy and Nutrients for the United Kingdom. Report on Health and Social Subjects No. 41. London: HMSO, 1991. This report provides the current recommendations for the United Kingdom. There are links to pages on the U.S. dietary reference intakes, including the 1999 and 2000 updates, at http://www.nal.usda.gov/ fnic/etext/000105.html (March 29, 2000). FAQs about DRIs and their interpretation appear at The National Academies Institute of Medicine at http://www4.nas.edu/IOM/IOMhome.nsf/ pages/FNB+FAQ+DRI and +Uses (March 20, 2000). U.S. Department of Agriculture Center for Nutrition and Policy and Promotion has a website at http://www.usda.gov/cnpp/.
3. http://www.nichd.nih.gov/milk/milk_fact.htm (March 28, 2000).
4. Norgan NG. Measurement and interpretation issues in laboratory and field studies of energy expenditure. Amer J Hum Biol. 1996;8:143-158. The methods for measuring energy expenditure are described and critically appraised. Variation and adaptation in energy expenditure are considered in the context of discriminating between these and honest error, particularly in activity where many of the problems arise.
6. Whitehead RG, Paul AA. Long-term adequacy of exclusive breast feeding: How scientific research has led to revised opinions. Proc Nutrit Soc. 2000;59:17-23. Improved nutritional and anthropo-metric guidelines are provided for the assessment of lactational adequacy and for when weaning may be initiated. These are based on revised dietary energy requirements.
7. Danielle PC, van Dusseldorp M, van Staveren WA, Hautvast JGAJ. Effects of macrobiotic diets on linear growth in infants and children until 10 years of age. Euro J Clin Nutrit. 1994;48(Suppl 1):S103-S112 or as the Waterlow and Schurch IDECG report.
8. Martorell R, Kettel Khan L, Schroeder DG. Reversibility of stunting: epidemiological findings in children from developing countries. Euro J Clin Nutrit. 1994;48(Suppl 1):S45-S57 or as the Waterlow and Schurch IDECG report.
9. Tanner JM. Foetus into Man: Physical Growth from Conception to Maturity, 2nd ed. Ware, UK: Castlemead Publications, 1989:130.
10. Adair LS. Filipino children exhibit catch-up growth from age 2 to 12 years. Journal of Nutrit. 1999;129:1140-1148.
11. Satyanarayana K, Nadamuni Naidu A, Narasinga Rao BS. Adolescent growth spurt among rural Indian boys in relation to their nutritional status in early childhood. Ann Hum Biol. 1980;7:359-365.
12. Martorell R, Scrimshaw NS. The effects of improved nutrition in early childhood: The Institute of Nutrition of Central America and Panama (INCAP) Follow-up Study. J Nutrit. 1995;125(Suppl 4):1027S-1138S or as an IDECG report.
13. Norgan NG. Chronic energy deficiency and the effects of energy supplementation. In: Schurch B, Scrimshaw NS. Chronic Energy Deficiency; Consequences and Related Issues. Lausanne: IDECG, 1987:59-76.
14. Allen LH. Nutritional influences on linear growth: A general review. Euro J Clin Nutrit. 1994;48(Suppl 1):S75-S89 or as the Waterlow and Schurch IDECG report.
15. Power C, Lake JK, Cole TJ. Measurement and long-term health risks of child and adolescent fatness. Inter J Obes. 1997;21:507-526. It is argued that anthropometric measures are practical for large-scale epidemiological studies. The child-to-adult adiposity relationship is well documented, although the prediction of adult adiposity is only moderate. This indicates that prevention should be population based rather than targeting fat children.
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