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Adult nutrition and cities - an international perspective
Noel W Solomons, MD
Centre for Studies of Sensory Impairment, Aging and Metabolism (CeSSIAM), Guatemala City, Central America

S A J Clin Nutr 2000 February Vol. 13 No 1.

As we stand on the verge of the 21st century, there is a temptation, and a need, to place the present century in historical perspective. The United Nations, founded in 1947 evolved a rhetoric that divided the nations into three worlds The ‘First World’ and ‘Second World’ were basically industrialised and located in temperate climes. The former comprised Japan, Australia, New Zealand, the nations of western Europe and North America, organised along the capitalist economic model; the latter comprised eastern Europe and the former Soviet Union with a socialist industrial model. The ‘Third World’ represented the rest of humanity. Most of it has a colonial history, having been part of the Empires of European colonial powers either into the 19th century, or into the post-World War II era of the mid 20th century. Most of it lies between the Tropics of Cancer and Capricorn. It has been sectioned into geographical blocs: Latin America, Asia, Oceania, and Africa.

Nutrition and human evolution
This topic is juxtaposed between issues of childhood (the "first age’) and the elder years (the ‘third age’), and it finds me addressing the stage in the middle, i.e. adulthood (or the ‘second age’). The human condition is part of the natural order, and what Nature is all about is the survival of species, and the diversity and interrelations of species. The raison d’etre of life is biodiversity and mutual species interdependence Organisms need food to satisfy their needs and this comes from other species. Throughout evolution, this has required the evolving of patterns of food and beverage consumption as an adaptation to the ecological niches in which Homo sapiens lived and the requirements for growth, maintenance and work by the human organism.1 This was especially important in the survival of individuals, but not all individuals survived to reproduce. The fact of an individual’s survival to reproductive age (second age, adulthood) is a signal to Nature that his or her genetic constitution may be superior to that of the peer who did not make it to procreative age. We cannot understand nutrition of any subgroup of the human population without placing it in the perspective of the evolutionary mandate of Nature.

Geography, demography and nutrition
Generally, at birth, there is a male to female ratio close to 1.0 (a slight male excess). How this proceeds after birth is a consequence of differential forces of mortality. In infancy, female children may be at greater risk of receiving inadequate care, or even of infanticidal practices. After adolescence, females are prone to death from obstetric causes, and men to accidental deaths or violent deaths in conflict. As such, male-excess or female-excess populations may become the rule for a specific society.

In terms of age, the contours of the age pyramid are often used to characterise the population. The base represents the juvenile group, the middle the adults, and the tip the elderly. The width of the various levels and the overall height of the pyramid define a population. What will be important for adult diet and nutrition will depend, from society to society, on the position the adult segment occupies within the age pyramid. In a situation of natural selection age pyramids have a broad base, a steep taper, and a short height. In the context of Hippocratic medicine and humanism, nutritional considerations go beyond (or go against) the imperative of natural selection. Considerations are related to maximised survival and maximal longevity.

With regard to geography, various patterns of the forces of natural selection or the penetration of humanistic philosophy (backed by technology) are found, depending upon the economic development of the region. Hence, the gamut of age pyramids discussed above is seen, and adults are either rare or abundant in relation to the other age groups. Geography also has an influence on the diet consumed. What is available in terms of fish and game (fauna) and forage (flora) determines dietary intake in traditional hunting settings, whereas the climate and soil conditions, along with cultural traditions versus modern agronomy, dictate what is cultivated as crops and raised as livestock in an agrarian society. Within a given area, the rural-urban cleavage directs what is preferred as the basis of the diet and what is available in any given season. As discussed below, diet and nutrition play both a determinant and a reactive role with regard to geography and demography, as what is eaten influences survival and health, and the pattern of the population age profile influences the demand for different items.

Worldwide versus global
Returning to the issue of an international perspective, I will borrow for nutrition what historians have used for decades, namely the differentiation between ‘world’ and ‘global’ history. The former is descriptive and comparative of the events of the ages; the latter connotes trends and movements that spread and converge from an epicenter(s). This view is more deterministic. Another way to make the transition from the historical context to the epidemiological one is in terms of science as reductionism (the former) or as holism (the latter). 2 This has often been discussed in the vernacular as ‘lumping’ (holism) and ‘splitting’ (reductionism).

On the reductionist scale, the specific public health measures that reflect the goals of our individualistic humanism may not be universal and congruent across the countries that make up a region, much less across the regions that make up the world. A meeting here in southern Africa reflects both a regional and linguistic bias: the European colonial history is largely related to Britain and Portugal. In 1992, an urban nutrition workshop was held in French-speaking Benin.3 A casual hypothesis might project that more similarities than differences would occur across the continent of Africa, at least below the Sahara. This denies important alternative hypotheses. As language derives from culture, and the cultural perspectives of the colonial entity may have forged the health and sanitation infrastructure, even neighbouring nations may differ in their diet, nutrition and health, based on whether British, French, Belgian, Portuguese or German colonial administrations had been involved in their past. Hence, between the neighbours of (formerly French) Togo and (formerly British) Gambia, marked difference may be present. Therefore, the perception of Africa from these two workshops – equatorial, French-speaking nations in 1993 and southern, English-speaking nations in 1999 – may involve striking contrasts.

On the holistic or synthetic side, one would analyse the topic in terms of any global trends. These need not be dominant yet, but should represent waves of consistent change. These could represent technology or fashions in nutrition and diet, patterns of disease, or advances in technology. Religious or philosophical movements in ascendancy or decline would also have this global context. Communication issues, forces of modernity, and economic resources may be factors determining the penetration of global movements, and Africa may be far behind other regions with regard to participating in the common ideas and practices.

A synthesis of the foregoing considerations means that both reductionism and holism have their respective roles to play in understanding issues of diet, nutrition and health. For this presentation, the international perspective has been interpreted more along the holistic track than the particular one. Some of the more obvious potential global trends that could influence adult nutrition in international perspective are listed in table I. These will be considered individually below.

Table I. Global trends

Urbanisation Shift from infectious disease to chronic disease mortality
The AIDS epidemic
The obesity epidemic
Synthetic and genetically-manipulated foods
The Internet

Nutrition as nutrient economics
The occurrence of nutrient deficiencies and excesses of nutrients obey laws of biological feasibility and circumstantial probability. By definition, deficiencies of all substances classified as ‘essential’ nutrients will result in clinical or functional manifestations. Not all such deficiencies will occur, however, when an oral diet is maintained, and some require extraordinary circumstances such as parenteral nutrition or antinutritional substances to provoke recognisable clinical consequences in humans. Our international perspective proceeds from an assumption that 75% of the world’s population live in developing countries or in depressed and deprived circumstances within industrialised nations, and that the remaining 25% have the privilege of relative affluence in their national or individual situations.

Famine, food insecurity, and energy adequacy
With regard to the original paradigm of nutrient adequacy, three states need to be addressed and defined. Famine is a situation in which there is too little food to feed the population dependent on that food supply. If divided equitably, almost all residents would take in less than their nutrient requirements. With unequal distribution of the inadequate supply, some people are able to obtain suprarequirement intakes of food and nutrients at the expense of the lives of those at the other extreme of the distribution scale. Food insecurity is the absence of ‘food security’. The latter has been defined as ‘access by all people at all times to enough food for an active, healthy life’. Energy adequacy has to do with the availability and accessibility of enough energy to cover the energy expenditure costs of individuals and households. Generally, energy expenditure on physical activity is less in urban settings than in rural ones as most of the employment activities for adult men require less physical work than is involved in field agriculture, while labour-saving devices involving electricity and running water, and shorter distances to walk to market or to visit neighbours reduces the energy requirements for women. Generally, energy adequacy for most urban dwellers is met by a combination of lower needs and more accessible food. Food is often the high-fat ‘empty calorie’ variety of packaged snacks and fast foods from street vendors.4 This sets up a bifurcation of energy adequacy with adequate micronutrient density and energy adequacy with micronutrient imbalance.

Micronutrient deficiencies in urban adults
A common denominator of three of the aforementioned conditions – famine, food insecurity and energy sufficiency with imbalance – is the risk of micronutrient deficiencies. Based on our knowledge of human biology, some generic generalities can be made concerning nutrient deficiencies of public health importance. Deficiencies of riboflavin, iron, vitamin B12 , folic acid, zinc and iodine are those most to adults as a whole. Particular dietary and ecological circumstances will condition their occurrence and expression. Residence in an urban area can often influence the likelihood of an endemicity of one or other of these nutrients.

Although it is widely stated that iron deficiency is the most common undernutrition problem on a worldwide basis, experience in Guatemala and common wisdom might point to riboflavin as being the number one problem for children and the elderly.6,7 Low consumption of milk and dairy products, the richest sources of vitamin B2 , is the principal mediating factor. Adult non-persistence of intestinal lactase limits the quantity of milk that can be consumed without provoking symptoms. The liability of riboflavin with regard to oxygen and light may reduce its content in fluid milk that is still sold in transparent glass and plastic containers. Such riboflavin deficiency is diagnosed on the basis of laboratory tests, usually depressed erythrocyte glutathione reductase activity in red cells, as it rarely becomes severe enough to produce the ocular and cutaneous manifestations of ariboflavinosis.

Specifically with regard to urban adults, no representative generalisations can be made. Greater chances of contact with dairy livestock in rural areas, the fresher quality of dairy products, and a tendency to consume fresh cheese in rural zones and processed cheese in cities would be reasons to suppose a paradoxical situation of better riboflavin status for the rural adult. At least in school children, we found a tendency for better riboflavin intakes and status in rural areas. 5

Iron deficiency may indeed be the most common nutrient deficiency in terms of the number of individuals affected, but not all age groups living in the same location and consuming a common diet are equally affected. Infants and preschool children, adolescents, and women in the reproductive years are the most vulnerable. Adult and elderly men and postmenopausal women seem to resist any tendency toward iron depletion.8 Obviously, menstruation and frequent pregnancies are a factor for adult nutrition as far as the female population is concerned. In addition to excessive iron loss, as in the two aforementioned situations, iron deficiency does not necessarily indicate an absence of total iron in the diet. Rather, it is the low biological availability of the mineral from diets high in edible plants and low in meat that accounts for the risk of iron deficiency.9

Not all iron deficiency leads to anaemia.10 It takes a certain interval for the red cell mass to shrink even after bone marrow reserves are depleted of iron. A series of functional deficits including impaired muscle metabolism, immune deficiency, and cognitive and alertness impairment have been ascribed to the state of iron deficiency without anaemia.

As urbanisation often involves greater consumption of red meat and separated fats, as documented in Beijing,11 the bioavailability of iron should improve with migration to the cities. To the extent that hookworm and Schistosomes are haemorrhagic parasites in the environment, urban locations provide the sanitation conditions to curtail the transmission of the parasitosis.

Vitamin B 12 status has been considered to be at highest risk in vegans and older persons at risk of atrophic gastritis. Recently, however, endemic vitamin B12 deficiency has been documented in child populations.12 Helicobacter pylori, the bacteria responsible for peptic ulcer disease, has been found to be pandemic throughout the world, with prevalences in some developing countries reaching 85%.13 In a certain percentage of infected individuals, so far not well defined, H. pylori leads to gastric atrophy and hypochlorhydria. This portends a potential epidemic of depressed gastric acid secretion in early life, with consequent impaired vitamin B12 nutriture at some point from adulthood to old age. Whether there is a rural-urban gradient in the susceptibility to H. pylori infection has not been fully determined. With regard to the quality-of-diet issues that might lead to compensatorily increased intakes of the vitamin, common sense would suggest that the higher intakes of meat and dairy products in urban settings might favour better vitamin B 12 nutriture in cities.

H. pylori may also be a factor in the complex area of folic acid nutrition and public health. Decreased acid secretion plays a role in folate malabsorption.14 A daily intake of 400 µg of folic acid is now recommended for women of childbearing age to reduce the risks of spina bifida and other neural tube defects occurring in their offspring,15 and in affluent countries to suppress circulating homocysteine concentrations with a concomitant alleviation of the risk factor for vascular diseases.16 To declare areas consuming lesser amounts of folic acid endemic for folic acid deficiency is,however, problematic owing to the fact that the neural tube defect may have an interaction with genetic polymorphisms which are most common in Caucasian populations, and to the philosophical distinction between an intake requirement and a recommended consumption for disease prevention.

Zinc has not been on the list of the major micronutrient deficiencies through the 50 years of post-war international nutrition. In 1973, Sandstead 17 wrote a speculative paper entitled ‘Zinc nutrition in the United States’. In 1993, Shrimpton 18 wrote a speculative paper entitled ‘Zinc deficiency — is it widespread but under-recognised?’. The problems with the diagnostic assessment of zinc status by laboratory means, both in the individual and populations, are legion.19 It is often only after a zinc supplementation intervention that a zinc-responsive condition can be revealed in a population. In North American women, zinc supplementation during pregnancy has improved birth weights.20 Like iron, the absolute amounts of zinc in the diet are not low, except in parts of the Amazon valley and northern China, but diets contain inhibitors that interfere with zinc absorption. Phytic acid from whole grain seed tissues, polyphenols (tannins) from coffee and tea, oxalates from green leaves and shoots and calcium are the primary inhibitors of zinc uptake. The factors of a more diversified and a more refined diet in urban cuisines would generally favour more — and more available — zinc. To the extent that acute infectious illnesses may be less frequent and intense in urban populations, the wasting of zinc could be minimised in Third-World cities.

Nutrient excess, overload and toxicity
Parcelsus warned that anything can be toxic when ingested sufficiently high doses. This applies to essential nutrients as well. In order for a harmful excess or overload of a nutrient to exist under usual conditions, however, the substance in question must have toxic consequences at an easily attained tissue or circulating concentration, and must accumulate faster than it can be metabolised or eliminated. Based on experience of human biology, energy (in the form of stored fat), two fat soluble-vitamins (Aand D), two water-soluble vitamins (B3 (niacin) and B6 (pyridoxine)), and several trace elements including iron, selenium, and copper can produce overload states in humans.

All of the mentioned nutrient-overload states can develop with the imprudent use of nutritional supplements. Of the mentioned nutrients, however, only two or three can produce overload under usual dietary circumstances. For example, except with a medicinal food like fish-liver oil, vitamin D excess from dietary sources is improbable. Over-use of of codliver oil or consumption of shark or polar bear liver would produce vitamin A excess from a food source. Naturally, the bioconversion of provitamin A carotenoids is regulated by the organism, so that gluttony involving carrot or papaya juice produces harmless carotenaemia but never hypervitaminosis A. In certain geological climes, selenium excess can develop based on consumption of crops and livestock raised in these selenium-laden regions, notably in Venezuela and China. Excess body energy accumulation (obesity) and excessive tissue iron reserves are the two nutrient overload states of dietary origin that merit serious consideration.

Obesity is a state of excessive storage of energy in the form of fat. Obesity or excess energy storage is perhaps the most widespread of the chronic diseases, the earliest in appearance during the lifespan, and one with a strong association with other chronic afflictions.21 As indicated by chronological monitoring over time, it is now clearly established that the body mass index or Quetlet, a proxy indicator for overweight and obesity in survey situations, has been rising world wide when controlling for age.22 Nutrient excess in urban adults is generally more common than in rural ones. Experience with Pacific islanders who migrated to metropolitan areas of New Zealand is one illustrative example.23

The ages from 35 to 64 years bracket the span of greatest prevalence of obesity.21 Moreover, adiposity increases through the lifespan from 20 to 64 years, peaking in the 50 to 64 ageband, and then decreasing with more advanced age. Obesity is an independent factor for mortality, and it is a concomitant in other life-threatening pathologies such as diabetes mellitus, hypertension and stroke, hyperlipidaemias and coronary ischaemic disease.24,25 An important review of the pandemic of obesity and its progression has been compiled by VanItallie.26 He accentuates the discrepancies in the definition of ‘obesity’ and its overlap and confusion with overweight. The former carries the connotation of excessive adiposity or over-fatness, whether or not weight-height relationships are distorted. Lustig and Wahlqvist 27 emphasise, moreover, the growing importance of the distribution of excess adipose tissue, with visceral fat deposited in the abdomen showing greater associations with morbid conditions than subcutaneous deposits. The body mass index (BMI), however, has fundamental limitations in reflecting excess fatness, including ethnicity-to-ethnicity inconsistency of the fatness associated with a given BMI, combined with a range of cut-off criteria for BMI that define obesity in its varying grades. All of this diagnostic uncertainty wrests precision from the obesity epidemiology and comparability among surveys around the world. All of these caveats and limitations notwithstanding, just using age-adjusted mean or median BMI values permits us to appreciate a dramatic incremental increase in body mass as a secular trend across the recent decades, and as part of the lifespan. Persons with high BMIs earlier in adulthood will tend to have more dramatic increases within their lifespans.

Iron deficiency is, in my estimation, the second most common deficiency state. It is also the second most frequent overload state. This results from genetic influences in interaction with diet, and exclusively from dietary exposure. Haemochromatosis is a genetic and heritable disorder of iron accumulation.28 In white populations of the USA and Australia, the gene prevalence of the homozygous state for haemochromatosis is estimated at 1 in 300, with the gene frequency for heterozygosity being about 1 in 10. In non-white societies, it is considered to be less prevalent, although exact statistics are not available. The notorious African haemosiderosis, commonly seen in Bantu men in Southern Africa who consume copious amounts of the radiator-brewed kaffir beer, has an interaction with a gene distinct from haemochromatosis.29 For the large majority of the world’s population none of these genetically determined iron-overload states is common; however, the lifelong accumulation of more than usual stores of iron has been explored as a potential factor for the induction or propagation of chronic illnesses.

Iron is the biological co-factor in all oxidative and free-radical generation processes. This provides a plausible mechanism for tissue and genetic damage from excess accumulation of iron stores. Hallberg et al.30 have argued that the regulation of iron status is guarded by the sentry of the intestinal absorption homeostasis and that humans will resist accumulation of iron beyond their corporal needs. However, the variance in serum ferritin as an index of total-body iron stores (or other biomarkers) has variously been implicated as an independent co-factor in all-cause mortality from cancer 31 and in the genesis of arterial wall plaque oxidation leading to thrombogenesis.32 The degree of relative risk remains disputed and controversial. That the residual dietary iron in the gastrointestinal lumen is an oxidising agent associated with colonic mucosal oxidation and potential carcinogenesis is a hypothesis worth pursuing as well.

An interesting interaction between a positive and an adverse nutritional state in the urban context is illustrated by Carrasco Sanez and co-workers 33 in a peri-urban slum (pueblo joven) on the outskirts of Lima, Peru. They observed a 22% rate of overweight in the population in a cross-sectional study. Anaemia rates (31%) were, curiously, lower in the overweight women than in the normal or underweight women (53%). One derivative hypothesis would be that the same predisposing factors for excess weight in this community were protective factors against iron deficiency.

Nutrition in the context of dietary patterns and health
Urban location and chronic diseases
Once the ‘epidemiological transition’ has passed a region (see below), most deaths are from cardiovascular disease and cancer. The assumptions of this presentation on the adult relate to the effects of nutrition and diet on susceptibility to chronic disease. Perhaps an important and valid generalisation is that mortality from chronic diseases is seen primarily in later life. In the case of the two principal categories of chronic diseases, cardiovascular disease (CVD) and cancer (CA), we assume that the middle years are the breeding-ground years, but as discussed below, juvenile diet and lifestyle may play a more important role than previously contemplated.

Epidemiology and demography
An equally safe generalisation is that life in the cities - as compared with life in the countryside of the same country - increases the risk of all forms of chronic disease (with the exception of those diseases related to chronic industrial exposure to uniquely rural endeavours such as agriculture, fishing, forestry, mining, etc.). Among the chronic diseases caused by exposures to rural pursuits, we can list cataract (ultraviolet wavelengths of sunlight), miner’s lung disease, and pesticide and herbicide toxicities. With regard to osteoarthritis (degenerative arthritis) the heavy weight-bearing exercise of rural lifestyle takes a toll on the weight-bearing joints.

Obesity as a chronic disease has been discussed above as both an illness in its own right and a conditioning factor for other maladies. CVD, which includes the family of coronary ischaemic disease, hypertension, cerebral vascular accidents (stroke) and peripheral arteriovascular disease, is seen in both rural and urban settings. In Costa Rica, it was shown that the risk factors for CVD increase incrementally as people were examined from more rural to more urban settings. Neoplasia or cancers are also considered more urban diseases, although tumours with specific links to the environmental hazards of agriculture, forestry and mining can afflict individuals working in those pursuits. Diabetes mellitus (DM) is increasing rapidly in incidence and prevalence in developing countries.34,35

Osteoporosis is another chronic ailment more common among urban dwellers; this is due to a differential excess of all of the recognised risk factors such as lower weight-bearing exercise, less sun exposure, lower calcium intake, higher animal protein intake, and higher rate of tobacco use.

With the exception of obesity and DM, the onset of clinical manifestations and mortality rates of CVD and CAare actually greater after age 60, i.e. in the elderly than in the second stage of adulthood. The question is that of initiation and promotion during earlier life, and whether that critical earlier life experience occurs during childhood or adulthood.

Nutrition in the context of dietary patterns
The traditional (and now conservative cum reactionary) view of ‘nutrition’ is that of obtaining and retaining specific essential and beneficial nutrients. It has only been in the last half century that the paradigm of dietary influence on chronic disease has emerged. The landmark was the 1953 paper by Keys 36 in which the so-called ‘cholesterol hypothesis’ for the origins of atherosclerosis was advanced. The comparable landmark for diet and CAcame with the paper by Doll and Peto 37 in which it was estimated that over 30% of all human malignant disease was attributable to diet. Lucas 38 has summed up this transition in the following manner: ‘In recent decades there has been a significant shift in thinking about nutrition from a preoccupation with meeting nutritional needs to a concern about its effects on health, including adult degenerative disease, cancer and cognitive function’. The evolution of what has come to be known as ‘nutritional epidemiology’ 39,40 has allowed a shift of the paradigm toward the pattern of dietary intake. This not only expands the vision to embrace nutrient insufficiency and nutrient excess, but also to include other influences from the diet. These are substances, nutrient or non-nutrient, and their interrelationships that can have disease-protective effects or disease-producing/ aggravating effects.

Powles and Ruth 41 have produced the most comprehensive review asking (and answering) the question of a relationship between dietary pattern and all-cause mortality. A companion chapter in the same book by Lustig and Wahlqvist 27 disaggregates the situation in terms of specific chronic, human diseases. Their master table takes each of 17 diseases and pathological conditions and reviews the predominance of evidence for protective and adverse associations with essential nutrients and the same associations with non-nutrient constituents of the human diet. This concept even involves the timing and size of individual repasts during the course of the day, i.e constant ‘grazing’ or occasional feasting.42 Again, in the paleo-comparative context of our hunter-gatherer ancestors, their meal pattern was probably the standard for human evolution.

The protective or provocative aspects of relationships of chronic diseases to diet begin at the level of foods. Diets high in fruits and vegetables and low in meats and fats are observed to be protective. Both scientists and public health professionals have been obsessed, however, with the individual components of the diet and their chemical nature. Phytosterols, dietary fibre, resistant starches, carotenoids, and flavonoids as well as some of the vitamins and minerals recognised as nutrients, have been the subject of speculation and investigation. Wine and other alcoholic beverages, when consumed in moderation have been identified as protective for CVD. Recently, the rate of absorption of the constituent carbohydrates (glycaemic index) has come under scrutiny; foods with more slowly absorbed glucose may be more ‘heart healthy’ over a lifetime

Diet and health finally involve food microbiology and classical toxicology. As a source of nutrients, food is appealing to bacteria as a culture medium. This leads to food-borne gastro-enteritides. In a broader context, the pathogens that attack our food source can pose a danger to us, as in trichinosis, bovine spongiform encephalopathy (BSE), and kuru, or through improper handling food can be the vehicle for the entry of human parasites such as the agents of intestinal parasitoses and cysticercoses. Classical toxicology deals with the diet as containing damaging components in the forms of toxins – inorganic, e.g. heavy metals; synthetic organic, e.g. dioxin, benzene; or natural organic, e.g. nitrosamine, mycotoxins and bacterial toxins, that produce acute food borne illness or more latent effects. This recapitulation reminds us that eating has always been necessary, but it has never been without hazard.

Influences from childhood – rather than adulthood – must be taken as a serious alternative consideration when dealing with both the dietary substances and patterns discussed above, and with the chronic disease outcomes. Professor David Barker 43 introduced an intriguing hypothesis based on long-term health outcomes in a cohort of men and women born in Sheffield, England, in the 1930s, namely that intra-uterine and early - infancy undernutrition leads to greater susceptibility to morbidity and mortality related to obesity, diabetes, hypertension, stroke, and coronary heart disease. The theoretical basis of this phenomenon is acquired metabolic programming in which the body tends to store and retain nutrients based on the need in early postconceptual life. Faced with dietary abundance, this hyper-retention conditions the consequences of caloric, fat, and sodium excess. The contents of a recent symposium on ‘The Effects of Childhood Diet on Adult Health’ at the American Society for Nutritional Sciences 38,44,-47 illustrate this point. From the point of view of developing countries, if the programming hypothesis 43 is valid, then an abrupt transition in one generation from in utero and early-life deprivation to luxus consumption in adult years, could pave the way for an onslaught of chronic disease consequences, many of which may have precocious onset in the middle years of life.

The history of dietary guidelines for the North American public from the time of Keys’s genesis of the paradigm in 1950 was reviewed by McNutt.48 The US Department of Agriculture has issued two editions of ‘Guidelines for the Americans’, one in 1990 and another in 1995. The World Cancer Research Fund and the American Institute for Cancer Research (WCRF/AICR) produced the most authoritative review of the influences of dietary and lifestyle factors on CA in Diet, Nutrition and Prevention of Cancer: An International Perspective in 1997, 49 along with a 14-point list of guidelines about diet, food preparation and handling, and lifestyle (Table II). Recently, a new field of assessment has been emerging, that of estimating the spontaneous concordance of a population’s behaviours with the enunciated provision of guidelines. This is typified by the exercise by Crane et al.50 which investigated the point-prevalence compliance of US residents with the 1995 dietary guidelines recommended by the US Department of Agriculture using archival data from household dietary surveys. We in Guatemala have turned attention to the WCRF/AICR recommendations for CAprevention by assessing the concordance of an individual’s total-diet food frequency records with the cancer-prevention goals.51

Genetic predisposition is a factor that both interact with diet and goes beyond dietary intake. Presumably, the expression of extreme genetic predisposition to manifest a chronic disease cannot be modified by any known dietary practices. Similarly, strong genetic resistance to the ill effects of injurious eating habits will overcome the pathogenetic influences of one’s dietary fare. For the majority of populations, however, whose risk is malleable and dependent on protective and provocative exposures from diet and lifestyle, adherence to recommendations by authoritative public health panels is a formula for better health through to adulthood and older age.

Table II. 14-point guideline for diet and lifestyle of the World Cancer Research Fund/American Institute for Cancer Research

  • Populations to consume nutritionally adequate and varied diets, based primarily on foods of plant origin.
  • Population average body mass indices throughout adult life to be within the range BMI 21 - 23, in order that individual BMI b maintained between 18.5 and 25.
  • Populations to maintain, throughout life, an active lifestyle equivalent to a physical activity level (PAL) of at least 1.75, with opportunities for vigorous physical activity.
  • Promote year-round consumption of a variety of vegetables and fruits, providing 7% or more total energy.
  • Avariety of starchy or protein-rich foods of plant origin, preferably minimally processed, to provide 45 - 60% total energy. Re sugar to provide less than 10% total energy.
  • Consumption of alcohol is not recommended. Excessive consumption of alcohol to be discouraged. For those who drink alcoh restrict it to less than 5% total energy for men and less than 2.5% total energy for women.
  • If eaten at all, red meat to provide less than 10% total energy,
  • Total fats and oils to provide 15% to no more than 30% total energy.
  • Salt from all sources should amount to less than 6 g/day (0.25 ounces) for adults.
  • Store perishable food in ways that minimise fungal contamination.
  • Perishable food, if not consumed promptly, to be kept frozen or chilled.
  • Establish and monitor the enforcement of safety limits for food additives, pesticides and their residues, and other chemical contaminants in the food supply.
  • When meat and fish are eaten, encourage relatively low temperature cooking.
  • Community dietary patterns to be consistent with reduction of cancer risk without the use of dietary supplements.S18

Global trends
Returning to the distinction between international as ‘worldwide’ and as ‘global’, Table I lists six topics that represent this author’s understanding of global trends relevant to adult nutrition.

Urbanisation
Cities have existed for 5 000 years, but it is only from the dawn of the Industrial Age that cities have become magnets for populations, drawing them to work in the factories. Only with the mechanisation and intensification of farming, however, could a small work force supply the food for an entire nation. Looked at conversely, this form of agriculture drove peasants off the land, and their only recourse was to migrate to urban areas.

From 1950 to the present day, the migration to, and natural growth of cities in developing countries has been accelerating; over 50% of the world’s population of less than 3 billion in 1950 lived in urban areas (communities of > 20 000 inhabitants). Within this context is the emergence of megametropolises, populations with more than 10 million residents. To place this in proportion, the president of Guatemala governs a total of 10 million citizens in a country of 109 000 km2. The mayors of Mexico City and Sao Paulo govern 25 and 21 million people respectively, and over 10 million residents are governed from the city halls of Tokyo, Seoul, Bombay, Calcutta, Jakarta, Delhi, Manila and Shanghai. 52

In terms of adult nutrition, migration to the city often entails changes in customary dietary practices. A greater diversity of foods is available. Diet is dependent on processed, commercialised foods. The availability of employment opportunities, rather than access to land for subsistence farming, is the leading factor in obtaining household foods. Invariably, meals prepared in the home are fewer in the urban milieu than in the countryside, and options ranging from fast foods and street foods to cafeterias present themselves, especially to schoolchildren and male heads of household at school and at work.

Shift from infectious disease to chronic disease mortality
The term ‘epidemiological transition’53 has been coined to describe the replacement of infections by chronic diseases as the cause of death in a population. Its basis in dietary influences, supported by lifestyle decisions and modulated by genetic constitution has been discussed above. What could be classified as a global trend is the situation in which the aetiology of mortality shifts from communicable diseases of early life to chronic degenerative diseases of later life.54 The young are differentially more susceptible to the endemic viral, protozoan, and bacterial diseases of humankind. That is why measles, pertussis, diphtheria and poliomyelitis are termed ‘diseases of childhood’. It is really respiratory infections and gastro-enteritides, however, that are quantitatively the major killing diseases of the pre-transition epidemiology. In areas in which malaria is hyperendemic, it is also a major cause of child mortality.

Cyclical plagues such as smallpox, bubonic plague and cholera also affect the middle of the age pyramid. A contemporary replica of the plagues of antiquity, AIDS has the potential to run the epidemiological transition off its course in those nations in which its transmission escapes preventive control.

The AIDS epidemic
The imponderable that could reverse a number of the global trends in this list and change the contours of the age pyramids of developing countries as well as the predictions for future trends in adult nutrition is the worldwide pandemic of HIV seropositivity and AIDS.55 The effect of advanced stage HIV disease has obvious and well-documented effects on nutritional status, producing the accelerated wasting that has given it the epithet ‘slim disease’ in Central Africa.56 Estimates that upwards of 1 in 4 of the adult population of some Africn and Asian nations are seropositive portend the death of huge numbers of adults around the world. Aside from the human tragedy, dislocation, economic disruption and burden of illness, the concern for the progression of chronic diseases is blunted by the attenuated progression of adults to older age status in the lifespan. To some extent the AIDS epidemic collides with the chronic degenerative disease epidemic. In some latitudes of the world the former may have the greater impact.

The obesity epidemic
It is undeniable that we are in the midst of an unprecedented worldwide obesity epidemic.57,58 On the Indian subcontinent many people have the body composition of chronic energy deficiency, but urban areas are experiencing endemic obesity The concept of the genetic and heritable passage of a ‘thrifty’ gene, governing a protein that promoted maximal conservation of energy during times when famine and scarcity were common, has been boosted by the identification of the obesity gene and the isolation of the peptide, hormone, leptin.59,60 To the extent that there has been adaptive polymorphism regarding leptin’s gene evolution, this could explain why an accelerated and exceptional move to adulthood obesity will be seen. That is, the availability of luxus consumption combined with a genetic predisposition to store energy will generate obesity if physical activity is not maintained at very high levels. The situation of the urban elite of Karachi, Delhi, Hyderabad and Colombo may also be a rebound to an adaptation that sustains their contemporary country cousins in their state of exaggerated thinness.61

Synthetic and genetically-manipulated foods
It has been documented that civilisation and staple crop agriculture have reduced the number of edible species consistently and regularly consumed to a virtual handful from the estimated 250 or more species consumed by historical hunter-gatherers of antiquity. No form of root, berry, succulent bark, bird, rodent, carnivore, insect, grub, slug or mollusc was off limits to the traditional hunter-gatherer. Diversity of diet was at its apogee in prehistoric, hunter-gatherer eras, reaching its nadir at the height of rural settled agriculture, as in the potato cultures of Peru with the Inca and the Irish of the early 19th centuryS20

The genetic manipulation of plants may be in the offing as a way to improve both the quantity and quality of plant foods for our growing terrestrial population. The ‘Green Revolution’ of the 1960s used hybridisation to increase crop yields and resistance to pests. With a growing interest in micronutrient density, plant breeding is once again being addressed. 62 This could mean either the conventional crossing of varieties to achieve hybrids of interest, as has been done in the beta-III (high-provitamin A) carrot, or by inserting and expressing genes, such as getting legumes to produce haem iron. Not only the adult population, but populations of all ages, are on the verge of being exposed to organic compounds which were never part of the evolutionary experience. This began with sweeteners such as cyclamates, and later aspartame. We have glucose and sucrose polymers in fat-substitute products with chemical linkages never observed in natural foods.

The Internet
The percentage of households with small computers connected to the Internet varies widely, with the more affluent countries far ahead of pre-industrialised countries. The situation varies, ranging from households with multiple PCs and television sets in every living space, to rural areas without electrification. Even within industrialised countries, computer literacy and cyberspace access varies among ethnic groups, with whites more involved than Hispanics or AfroAmericans in the USA. The use of the Internet is destined to increase, as may the dissimilarities in terms of Internet usage among cultural and ethnic groups. The information on the Internet and the products that can be advertised there can reach millions of ‘net surfers’ across the globe. Will this be useful information or misinformation? It has been argued that the authority of ‘scholarship’ will be weakened as the dominance of the established media and academic literature give way to the unfiltered opinion that anyone can place on their web page. A common theme on the internet is health and dietary advice. A potentially adverse, if not devastating, outcome of mass electronic communication could be the proliferation of unscientific and harmful practices.

Implications for research on adult nutrition
There are two urgent implications for consideration in terms of ‘world’ and ‘global’ adult nutrition: (i) public health; and (ii) human nutrition research. Based on the present treatise, these concern four areas: (i) avoidance of nutrient deficiency; (ii) avoidance of excessive nutrients; (iii) maximisation of protective substances; and (iv) minimisation of noxious substances. It is my contention that public health measures will only be strengthened by the advance of sound research. With regard to theory and principles, we require the global perspective to guide us to the health solutions that emanate from the Hippocratic paradigm. However, for a public health application we need both to extend our understanding of the waves of change, specifically in urban populations, and to learn how to account for the specificity and diversity. We nee to incorporate in our remedial and preventive tactics the manner in which particular, exceptional and transitional situations are to be addressed in given locales, with a given ethnicity, and with a determined pre-migration evolution within the ecosystem niche.

Cumulative comparative phenomenology
The middle years have appeared to be epidemiological doldrums, with traumatic, violent and accidental death and obstetric complications in childbirth outstripping pathologies as a cause of mortality. From the perspective of gerontology, however, this might be viewed as the calm before the storm The dietary pattern is the essential focus. What passes the lips in terms of variety and diversity, specific nutrients and non-nutrients, and meal patterns needs to be documented. To the extent that biomarkers of ageing and of pre-expressed and pre-clinical disease are validated, these can be coupled to the diet-pattern research.

Synthesis to theory
It is a basic tenet of the dialectical scientific method that nothing can be proved to be true. We can only demonstrate that things are not true. Hence, scientific ‘knowledge’ in biology is based on a series of enduring theories that explain the operations of nature. The end for the scientist is to contribute to theory development, but also to test theories. For countries in epidemiological transition throughout the developing world, the Barker hypothesis 43 is a major theoretical precept. Is it the nutrition and growth of the child in utero and during the early life period that dominates the acquired risk and the cumulative disease experience (Table III)? If so, how remediable is the determination? And do eating habits and diet content during adulthood modify the process? The now classic nutritional epidemiological studies, namely the Nurses’ Health Study and the Physicians’ Health Study have illustrated a series of presumably causal, protective or deleterious associations, with odds ratios to the order of 0.8 - 1.2. 39 This means that one has about a 20% deficit or excess probability of a disease being in the highest percentiles for consumption of a food or substance as compared with the other extreme.

Table III. Programme of the American Society for Nutritional Sciences Symposium (1997) on ‘The Effects of Childhood Diet on Adult Health’

Roberts SB, McDonald R. The evolution of a new research field:metabolic programming by early nutrition.
Lucas A. Programming by early nutrition. An experimental approach.
Birch LL. Psychological influences on the childhood diet.
Dietz WH. Childhood weight affects adult morbidity and mortality.
Sawaya AL, Grillo LP, Verreschi I, Carlos de Silva A, Roberts SB. Mild stunting is associate with higher susceptibility to the effects high fat diets: Studies in a shantytown population in Sao Paulo, Brazil.

Multicentre studies
The way to build a data base that can lead to an understanding of what is casual and what is global is by taking a broad comparative look at the international situation. Several approaches have been used. One involves meta-analysis, assembling the totality of spontaneously conducted and published studies and assessing their consistency and the dominant trend. In general, only one or two outcome variables of interest will be common in the meta-analysis approach. In a prospective way, multicentre studies are useful in peeling away our ignorance regarding nutrition, its determination and its relation to health. In the area of population and public health gerontology, multicentre studies have surged. They began with the SENECA-EURONUT study63 which used a common diet, nutrition, health, function, demography protocol to study 19 sites in 12 European countries. This was followed by the Food Habits in Later Life (FHILL) study, executed in 9 nations by the Committee on Ageing and Nutrition of the International Union of Nutritional Sciences.64 All of these studies pertain to the elderly. The general lack of interest in the midlife adult has led to a dearth of studies on this age group.

The CRONOS protocol (Cross-Cultural Research in Nutrition in Older Subjects) has a special relevance to this meeting as it originated within the International Union of Nutrition Sciences (IUNS) Committees on Urbanisation and Nutrition and Ageing and Nutrition. The origins of this study have been documented in a supplement to the Food and Nutrition Bulletin.65 Its primary thrust is the vertical comparison, but the design involves enrolment of persons aged 25 - 35 years from the rural peasant class, the urban poor, and the urban middle-class elite. Perhaps this body of data, analysed in its own right, might produce a substrate for addressing concerns about the‘forgotten’ adult as well. At least after a series of CRONOS experiences, one could make a preliminary analysis to assess the advances that might be made along that route.

In conclusion and merging theory to practice the real frontier will come with the resolution of the questions. The goal is high quality of disease-free life and successful and fulfilling ageing. This is the essence of preventive health. What to eat, when and how much, what to avoid, and what the benefits for one’s individual function and longevity will be the products of the research challenge. Strategic and ethical questions will emerge with the question of how collective and communal or individualised and particular to make the interventions. The adult years are not as dynamic in terms of health instability as childhood or older age; however, the study of this bridging period is the stepping stone to an understanding that links all of the determinants of health throughout the lifespan.

References

  1. Eaton SB, Konner M. Paleolithic nutrition: A consideration of its nature and current implications. N Engl J Med 1985; 312: 283-289.
  2. Gross R, Solomons NW. Tropical Urban Nutrition. Sonderpublikation der GTZ, No 197 Escborn: German Agency for Technical Cooperation, 1987.
  3. Nago MC, Hounhouigan JD, de Konig F, Gross R, eds. La Situation Alimentaire et Nutritionnelle dans les Zones Urbaines en Afrique. Report of a Workshop. Porto Novo Centre National de Production de Manuels Scolares, 1993.
  4. Sujatha T, Shatrugn V, Rao GVN, Reddy GCK, Padmavathi KS, Vidtasagar P. Street food: An important source of energy for the urban worker. Food and Nutrition Bulletin 1997; 18:337-346
  5. Solomons NW, Haskell M, Bulux J, Molina S. Nutrition and health condition of periurban preschool and school populations of Guatemala City. In: Hautvast JGAG, ed Urban Nutrition. Pre-school Children. Ede: Holland, Foundation for the Advancement of the Knowledge of the Nutrition of Mother and Child in Developing Countries, 1990: 119-150.
  6. Boisvert WA, Castañeda C, Mendoza I, et al. The prevalence of riboflavin deficiency among Guatemalan people and its relation to milk intake. Am J Clin Nutr 1993; 58: 85-90
  7. King JE, Mazariegos M, Valdez C, Castañeda C, Solomons NW. Nutritional status indicators and their interaction in rural Guatemalan elderly. A study in San PedroAyampuc. Am J Clin Nutr 1997; 66: 795-789.
  8. Yip R. Iron deficiency. Contemporary scientific issues and international programmatic approaches. J Nutr 1994; 124: 1479S-1490S.
  9. Viteri FE. Iron supplementation for the control of iron deficiency. Nutr Rev 1997; 55: 195-209
  10. Cook JD, Finch CA . Assessing iron status of the population. Am J Clin Nutr 1979; 32: 2115-2119.
  11. Fu P, Zhang H, Siew SM, et al. Food intake patterns in urban Beijing Chinese. Asia pacific Journal of Clinical Nutrition 1998; 7: 117-122.
  12. Allen LH, Rosado JL, Casterline JE, et al. Vitamin B 12 deficiency and malabsorption are highly prevalent in rural Mexican communities. Am J Clin Nutr 1995; 62: 1013-1019.
  13. Castro LD, Coehlo LG. Helicobacter pylori in South America. Can J Gastroenterol 1998; 12: 509-512.
  14. Russell RM, Krasinski SD, Samloff IM, Jacob RA, Hartz SC, Brovender SR. Folic acid malabsorption in atrophic gastritis: compensation by bacterial folate synthesis. Gastroenterology 1986; 91: 1476-1482.
  15. Anonymous. Folic acid fortification. Nutr Rev 1996; 54: 94-95.
  16. Pieztrik K, Breonstrup A. Vitamin B12, B6 and folate as determinants of homocysteine concentration in the healthy population. Eur J Pediatr 1998; 157: suppl 2, S135-S138
  17. Sandstead HH. Zinc nutrition in the United States. Am J Clin Nutr 1973; 26: 1251-1260
  18. Shrimpton R. Zinc deficiency – is it widespread but under-recognized? SCN News 1993; 9: 24-27.
  19. Solomons. On the assessment of zinc and copper nutriture in man. Am J Clin Nutr 1979; 32: 586-871.
  20. Goldenberg RL, Tamura T, Neggers Y, et al. The effect of zinc supplementation on pregnancy outcome. JAMA 1995; 274: 463-468.
  21. Gill TP, Antipatis VJ, James WPT. The global epidemic of obesity. Asia Pacific Journal of Clinical Nutrition 1999; 8: 75-81.
  22. Pelletier DL, Rahn M. Trends in body mass index in developing countries. Food and Nutrition Bulletin 1998; 19: 223-238.
  23. Simmons D, Mesui J. Decisional balance and stage of change in relation to weight loss exercise and dietary fat reduction amng Pacific Islands people. Asia Pacific Journal of Clinical Nutrition 1999; 8: 39-45.
  24. VanItallie T. Health implications of overweight and obesity in the United States. Ann Intern Med 1985; 103: 938-988.
  25. Pi-Sunyer FX. Medical hazards of obesity. Ann Intern Med 1993; 119: 655-660.
  26. VanItallie TB. Prevalence of obesity. Endocrinol Metab Clin North Am 1996; 25: 887-905
  27. Lustig JR, Wahlqvist ML. Disease-orientated preventive nutrition. In: Wahlqvist ML, Vobecky JS, eds. Medical Practice of Preventive Nutrition. London:Smith-Gordon, 1994: 91-118
  28. Powell LW, Kazwinska E, Halliday JW. Primary iron overload. In: Brock JH, Halliday JW, Pippard MJ, Powell LW, eds. Iron Metabolism in Health and Disease . London: WB Saunders 1994: 227-270.
  29. Gordeuk V, Mukiibi J, Hasstedt SJ, et al. Iron overload in Africa: interaction between a gene and dietary iron content. N Engl J Med 1992; 326: 95-100S22
  30. Hallberg L, Hulten L, Gromatkovski E. Iron absorption from the whole diet in men. How effective is the regulation of iron absorption? Am J Clin Nutr 1997; 66: 347-356.
  31. Stevens RG, Jones DY, Micozzi MS, Taylor PR. Body iron stores and the risk of cancer. N Engl J Med 319: 1047-1053.
  32. Salonen JT, Nyyssonen K, Korpela H, Tuomilehto J, Seppanen R, Salonen R. High stored iron levels are associated with excess risk of myocardial infarction in eastern Finnnish men. Circulation 1992; 86: 803-811.
  33. Carrasco Sanez N, Door de Ubillas RM, Salvatierra Guillen I. Increasing Women’s Involvement in Community Decision-Making: AMeans to Improve Iron Status. Research report series 1. Washington, DC: International Center for Research on Women, 1998.
  34. Samal KC, Tripathy BB, Mohan V. Consensus statement:International workshop on types of diabetes peculiar to tropics – 1995, Cuttack , India. Diabetes Research Group . J Diabetes Complications 1997; 11: 314-318.
  35. Tripathy BB, Samal KC. Overview and consensus statement on diabetes in tropical areas. Diabetes Metab Rev 1997; 13: 63-76.
  36. Keys A. Atherosclerosis:a problem in the new public health. Journal of the Mount Sinai Hospital 1953; 20: 118-153.
  37. Doll R, Peto R. The causes of cancer . Journal of the National Cancer Institute 1981; 66:1191-1208.
  38. Lucas A. Programming by early nutrition:An experimental approach. J Nutr 1998; 128: 401S-406S.
  39. Willett W, ed. Nutritional Epidemiology. 2nd ed. New York:Oxford University Press, 1998.
  40. Margetts BM, Nelson M, eds. Design Concepts in Nutritional Epidemiology. Oxford:Oxford Medical Publications, 1991.
  41. Powles JW, Ruth D. Diet-mortality associations. In: Wahlqvist ML, Vobecky JS, eds. Medical Practice of Preventive Nutrition. London: Smith-Gordon, 1994: 75-90.
  42. Danone Research Centers. Patterns of Food Intake in Schoolchildren. Nutrition and Health Collection. Paris: Irvinn Editions, 1997.
  43. Barker DJ. Maternal nutrition, fetal nutrition, and disease in later life. Nutrition 1997; 13: 807-813.
  44. Roberts SB, McDonald R. The evolution of a new research field:Metabolic programming byearly nutrition. J Nutr 1998; 128: 400S.
  45. Birch LL. Psychological influences on the childhood diet. J Nutr 1998; 128: 407S-410S.
  46. Dietz WH. Childhood weight affects adult morbidity and mortality. J Nutr 1998; 128: 411S-414S.
  47. Sawaya AL, Grillo LP, Verreschi I, Carlos de Silva A, Roberts SB. Mild stunting is associated with higher susceptibility to the effects of high fat diets:Studies in a shantytown population in Sao Paulo, Brazil. J Nutr 1998; 128: 415S-420S.
  48. McNutt K. Dietary advice to the public. Nutr Rev 1980; 38: 353-360.
  49. World Cancer Research Fund/American Institute for Cancer Research. Diet, Nutrition and Cancer Prevention: A Global Perspective. London: WCRF/AICR, 1997.
  50. Crane NT, Hubbard VS, Lewis CJ. National nutrition objectives and the Dietary Guidelines for Americans. Nutrition Today 1999; 33: 49-58
  51. Valdes-Ramos R, Solomons NW, Mendoza I, Anderson AS. Concordance of rural Guatemalan diets with the cancer prevention guidelines of the World Cancer Research Fund: Estimates from existing dietary intake instrument data. FASEB J 1999; 13A: 465.19 (abstr).
  52. Solomons NW. Urban nutrition:Overview. In: Sadler M, Strain JJ, Caballero B, eds. Encyclopedia of Human Nutrition. London: Academic Press 1999; 1904-1909.
  53. Murray CJL, Lopez AD. Global Comparative Assessments in the Health Sector. Geneva: World Health Organisation, 1994.
  54. Forrester T, Cooper RS, Weatherall D. Emergence of Western diseases in the tropical world: the experience with chronic cardiovascular diseases. Br Med Bull 1998; 54: 463-473.
  55. Grant AD, de Cock KM. The growing challenge of HIV/AIDS in developing countries. Br Med Bull 1998; 54: 369-381.
  56. Tomkins A. Malnutrition and risk of infection. In: Wahlqvist ML, Trushwell AS, Smith R, Nestel PJ, eds. Nutrition in a Sustainable Environment. Proceedings of the XV International Congress on Nutrition. London: Smith-Gordon 1994: 665-668.
  57. Popkin BM, Bray G. Dietary fat does affect obesity! Am J Clin Nutr 1998; 68: 1157-1173.
  58. Coulston AM. Obesity as an epidemic: facing the challenge. J Am Diet Assoc 1998; 98: suppl.10, S6-S8.
  59. Freuhbeck G, Jebb SA, Prentice AM. Leptin: physiology and pathophysiology. Clin Physiol 1998; 18: 399-419.
  60. Auwerx J, Staels B. Leptin. Lancet 1998; 351: 737-742.
  61. Popkin BM, Richards MK, Monteiro CA. Stunting is associated with overweight in children in four nations that are undergoing the nutrition transition. J Nutr 1996; 126: 3006-3013.
  62. Bouis H. Enrichment of food staples through plant breeding: A new strategy for fighting micronutrient malnutrition. Nutr Rev1996; 54: 131-137.
  63. De Groot LCPGM, van Staveren WA, Hautvast JGAJ, eds. EURONUT - SENECA: Nutrition and the elderly in Europe. Eur J Clin Nutr 1991; 45: suppl. 3, S1-S127.
  64. Wahlqvist ML, Davies L, Hsu-Hage BH-H, Kouris-Blazos A, Scrimshaw NS, Steen B. Food habits in later life: A cross-cultural approach. CD-ROM electronic edition. Melbourne: United Nations University, 1996.
  65. Gross R, Solomons NW, Barba CVC, de Groot CPGM, Khor G-L, eds. The development of a protocol to study the interaction of nutrition, ageing and urbanization in developing countries: Cross-Cultural Research on the Nutrition of Older Subjects (CRONOS). Food and Nutrition Bulletin 1998; 18: 218-219.