One in three children in Britain lives in poverty (households whose income was less than 50 % average earnings). Low income is associated with poor nutrition at all stages of life, from lower rates of breast-feeding to higher intakes of saturated fatty acids and lower intakes of antioxidant nutrients. Moreover, there is increasing evidence that poor nutrition in childhood is associated with both short-term and long-term adverse consequences such as poorer immune status, higher caries rates and poorer cognitive function and learning ability. These problems arise primarily because parents do not have enough money to spend on food, not because money is being spent unwisely. Policy options to improve the dietary health of poor children include: giving more money to the parents by increasing Income Support (social security) payments, providing food stamps or vouchers, and using food budget standards to inform the levels of income needed to purchase an adequate diet; feeding children directly at school (not only at lunchtime but also at breakfast or homework clubs), by providing free fruit at school, and by increasing entitlement to free food amongst children living in households with low incomes; improving access to a healthy and affordable diet by first identifying ‘food deserts’ and then considering with retailers and local planners how best to provide food in an economical and sustainable way. The value of using food budget standards is illustrated with data relating expenditure on food to growth in children from ‘at-risk’ families (on low income, overcrowded, headed by a lone parent or with four or more children under 16 years of age) living in a poor area in London. Lower levels of expenditure are strongly associated with poorer growth and health, independent of factors such as birth weight, mother’s height, or risk score. The present paper provides evidence that supports the need to review Government legislation in light of nutrition-related inequalities in the health of children.

Dietary guidelines for health promotion and disease prevention in the USA recommend a consumption pattern based largely on grains, fruit and vegetables, with smaller amounts of meat and dairy foods, and even smaller amounts of foods high in fat and sugar. Such diets are demonstrably health promoting, but following them raises ethical issues related to the role of nutritionists in advising the public about healthful dietary choices, as well as to the role of the food industry in food production and marketing. In the USA a shift towards a more plant-based diet would affect the economic interests of producers of food commodities, food products and meals prepared outside the home; it would also affect the environment, food prices, trade with other countries (developing as well as industrialized) and relationships among the food industry, government agencies (domestic and international) and food and nutrition professionals. In a free-market economy any dietary choice has consequences for food producers. Thus, considerations of ethical dilemmas in choosing healthful diets suggest that food choices are political acts that offer opportunities for all parties concerned to examine the consequences of such choices and ‘vote with forks’.

While being underweight or stunted is recognized as an important risk factor for increased prevalence and severity of infection and high mortality rates, there is increasing evidence for an independent role for micronutrient deficiency. Improving vitamin A status reduces mortality among older infants and young children and reduces pregnancy-related mortality; it also reduces the prevalence of severe illness and clinic attendance among children. Improving Zn status reduces morbidity from diarrhoeal and respiratory infection. Treatment of established infection with vitamin A is effective in measles-associated complications, but is not as useful in the majority of diarrhoeal or respiratory syndromes. Zn supplements, however, have significant benefit on the clinical outcome of diarrhoeal and respiratory infections. Concerns that Fe supplements might increase morbidity if given in malarious populations appear to be decreasing, in the light of new studies on Fe supplements showing improved haemoglobin without an increase in morbidity. Breast-feeding, well known to protect against diarrhoea, is also important in protecting against respiratory infection, especially in the young infant. Transmission of human immunodeficiency virus (HIV) in breast milk is recognized, but new data showing reduced transmission in infants who receive exclusive breast-feeding rather than mixed feeding reinforces the importance of promoting this practice in areas where environmental contamination precludes the safe use of other infant feeding regimens. The presence of subclinical mastitis, now recognized to occur in approximately 20 % of mothers in several developing countries, has been shown to increase the concentration of HIV in breast milk. Preliminary findings suggest that the prevalence of subclinical mastitis is reduced by dietary supplements containing antioxidants. Governments and international agencies now have a strong scientific basis to be much more active and innovative in the introduction of focused nutrition interventions especially micronutrients, for the control of infection.

Poor growth performance during infancy and early childhood is a frequent fact of life in most developing countries. Work in The Gambia has demonstrated that more than 43 % of observed growth faltering during the first 15 months of life can be explained by the presence of a mucosal enteropathy in the small intestine. Within communities the illness is very common: in the area investigated more than 95 % of infants above 8 months of age were affected, and on average they suffered a growth-limiting enteropathy for more than 75 % of their first year of life. Two mechanisms of weight loss have been defined. First, partial villus atrophy reduces absorption and digestion of lactose and probably other nutrients. Second, and more importantly, damage to the mucosal barrier allows translocation of macromolecules into the mucosa and blood, triggering both local and systemic immune and inflammatory mechanisms. Given the severity of the enteropathy it is not surprising that infants fail to grow at a normal rate. Recent findings suggest that these lesions continue throughout childhood and into adulthood. Thus, a persistence of chronic, local and systemic inflammation throughout childhood may be responsible for continued poor growth during this period. Although the nature of the enteropathy and the mechanisms of growth failure have been defined, the factors involved in the initiation and persistence of the intestinal lesion remain uncertain, making clinical management difficult. More work is clearly required to elucidate these factors and to define interventions to prevent or treat the enteropathy.

Since the 19th century there have been clearly documented secular trends to increasing adult height in most European countries, with current rates of 10–30 mm / decade. Over the same period menarcheal age has also fallen steeply, but has now stabilized at approximately 13 years and may be rising again. Height trends tend to be greater in childhood than in adulthood due to the associated advance in maturation, but no trends are apparent before the age of 2 years. In particular, birth-weight trends are small and different in shape from height trends. The adult height trend matches that at age 2 years, so that the increment in adult height has already been achieved by age 2 years. To try to identify factors relating to the secular trend, increased height gain in late infancy is hypothesized to be equivalent to a reduction in stunting, and stunting is thought to be caused by impaired growth in the long bones of the leg in later infancy. Leg growth may be regulated by the expression of growth-hormone receptors on the growth plates, which it is hypothesized are susceptible to the interaction between concurrent nutrition and the nominal growth rate set during pregnancy. The timing of menarche is also likely to be determined by some growth factor operating near the time of birth, which also affects later weight, but not height.

The acquisition of increased adipose tissue mass in man occurs during prolonged periods of positive energy balance. Normally, energy homeostasis in children and adults is regulated strictly and the energy stores are kept within the defined age-dependent physiological range. Susceptibility to definitive increases in the level of energy balance during times of reduced energy consumption or increased energy intake, leading to changes in body composition and/or changes in relative body weight, seems to be genetically determined. Although at present much information on the regulation of energy homeostasis and related unfavourable factors exists from animal studies, knowledge of the regulation of energy balance in human subjects is still insufficient. Some evidence on relevant factors involved in the regulation of energy balance in man has been obtained from epidemiological data, as well as from studies of patients with rare monogenetic forms of obesity. In the present article a special focus will be put on the regulation of body energy stores at the level of the adipose tissue, with emphasis on the regulation of human adipocyte differentiation. In addition to the currently intensive scientific interest in the central regulation of energy homeostasis in man, there is sufficient evidence to support the idea that the acquisition of an increased adipose tissue mass is also dependent on the susceptibility of pre-adipocytes to proliferate, to differentiate or to enter into apoptosis.

The nutritional condition of children with human immunodeficiency virus (HIV) infection continues to be a problem both in developed and developing countries. HIV-infected children grow below normal standards in both height and weight when compared with HIV-exposed non-infected children. These patterns persist over time. It is possible that acute infectious episodes and increased HIV viral burden contribute to decrements in all growth variables. Potential aetiologies for abnormal growth include inadequate dietary intake, gastrointestinal malabsorption, increased energy utilization and psycho-social problems. It is likely that all these factors contribute to the growth problems of these children to some extent. With the development of protease inhibitor anti-retroviral therapy and highly-active anti-retroviral treatment regimens, children with HIV infection in developed countries are living longer with a chronic illness. New nutritional problems have arisen with the development of the fat redistribution syndrome or lipodystrophy. Emerging problems are now being recognized, with the development of insulin resistance and truncal obesity which may potentially lead to premature cardiovascular disease.

Adipose tissue is a major source of metabolic fuel. This metabolic fuel is stored in the form of triacylglycerol. Lipolysis of triacylglycerol yields non-esterified fatty acids and glycerol. In human subjects in vivo studies of the regulation of lipid metabolism in adipose tissue have been difficult because of the heterogeneous nature of the tissue and lack of a vascular pedicle. In the last decade the methodology of study of adipose tissue has improved with the advent of the anterior abdominal wall adipose tissue preparation technique and microdialysis. These techniques have demonstrated that lipid metabolism in adipose tissue is finely coordinated during feeding and fasting cycles, in order to provide metabolic fuel when required. Lipolysis takes place both in extracellular and intracellular space. The extracellular lipolysis is regulated by lipoprotein lipase and the intracellular lipolysis is regulated by hormone-sensitive lipase. In pathophysiological conditions such as trauma, sepsis and starvation profound changes are induced in the regulation of lipid metabolism. The increased mobilization of lipid fuel is brought about by the differential actions of various counter-regulatory hormones on adipose tissue blood flow and adipose tissue lipolysis through lipoprotein lipase and hormone-sensitive lipase, resulting in increased availability of non-esterified fatty acids as a source of fuel. In recent years, it has been demonstrated that adipose tissue produces various cytokines and these cytokines can have paracrine and endocrine effects. It would appear that adipose tissue has the ability to regulate lipid metabolism locally as well as at distant sites such as liver, muscle and brain. In future, it is likely that the mechanisms that lead to the secondary effects of lipid metabolism on atheroma, immunity and carcinogenesis will be demonstrated.

In healthy subjects the metabolic response to starvation invokes regulatory mechanisms aimed at conservation of protein mass. This response is characterized by a decrease in energy expenditure and a progressive decrease in urinary N excretion. Many non-endocrine diseases induce anorexia and a decrease in food intake. However, in contrast to the metabolic reaction to starvation in healthy subjects, anorectic patients with serious diseases have increased energy expenditure and protein catabolism, associated with profound neuroendocrine alterations. These neuroendocrine changes are induced by two mechanisms. First, afferent nerves inform the central nervous system of tissue injury which results in neuroendocrine activation. Second, tissue injury stimulates the production of inflammatory mediators, which in turn results in neuroendocrine and metabolic effects. Although these metabolic changes enable the organism to survive short-lasting diseases by using endogenous substrates, in protracted serious diseases these changes will result in loss of functioning protein mass and may endanger survival. Moreover, tissue injury alters the metabolic responses to nutrition, reflected in the persistence of catabolism as long as serious tissue injury remains.

The trace element and vitamin requirements of severely-ill injured patients depend on a complex interaction of the status of the patient at the time of admission, ongoing losses and the potential benefit of supplying large amounts of individual micronutrients. Characteristic clinical deficiency states are now uncommon, but subclinical deficiency is of growing concern. The main effects of subclinical deficiency are: (1) an altered balance of reactive oxygen species and antioxidants, leading to oxidative damage of polyunsaturated fatty acids and nucleic acids, and possibly to increased activation of the transcription factor nuclear factor-κB, with increased production of pro-inflammatory cytokines; (2) impaired immune function with increased likelihood of infectious complications. Laboratory tests to optimize intake in such critically-ill patients lack sensitivity and specificity, this situation being made worse as a result of the acute-phase response. Recent studies have indicated the clinical benefit of providing large amounts of certain micronutrients in burned and head-injured patients. Further clinical studies are now required to define optimal levels of provision in different disease states, with a particular emphasis on markers of tissue function and clinical outcome.

While many studies have reported that providing parenteral nutrition (PN) can change nutritional outcomes, there are limited data that demonstrate that PN influences clinically-important end points in critically-ill patients. The purpose of the present paper is to systematically review and critically appraise the literature to examine the relationship between PN and morbidity and mortality in the critically-ill patient. Studies comparing enteral nutrition (EN) with PN and studies comparing PN with no PN were reviewed. The results suggest that EN is associated with reduced infectious complications in some critically-ill subgroups. PN, on the other hand, is associated with increased morbidity and mortality in critically-ill patients. When nutritional support is indicated, EN should be used preferentially over PN. Further studies are needed to define the optimal timing and composition of PN in patients not tolerating sufficient EN. Strategies to optimize EN delivery and minimize PN utilization in critically-ill patients are indicated.

Despite a marked increase in the prescription of oral nutritional supplements (ONS) in the community (Department of Health, 1991–7), there is still uncertainty about the value of their use in patients with different diseases. To answer questions about the effects on ONS on body weight and structure, spontaneous food intake and body function, a critical systematic review was undertaken (Stratton & Elia, 1999a). Eighty-four trials were reviewed (forty-five randomized, thirty-nine non-randomized; 2570 patients; diagnoses including chronic obstructive pulmonary disease, Crohn’s disease, cystic fibrosis, human immunodeficiency virus and acquired immune deficiency syndrome and cancer). Most studies (83 %) were conducted in patients living at home. The supplements were typically mixed macronutrients in liquid form, providing < 0.42–10.5 MJ/d for 1 week–2 years. The studies reviewed in patients with predominantly chronic conditions living in the community suggested that: (1) ONS produce demonstrable clinical (including functional) benefits, but the nature and extent of these benefits varies with the underlying chronic condition; (2) ONS increase total energy intake with > 50 % of the energy from ONS typically additional to that from habitual food intake; (3) improvements in body weight, total energy intake and body function following ONS appear to occur more frequently in individuals with a BMI < 20 kg/m2 than in those with a BMI > 20 kg/m2.

The growing interest in the role of phyto-oestrogens in human health has prompted scientists to evaluate the risk : benefit which would result from consuming high levels of these compounds at different stages of the life cycle. These compounds have been shown to exert a wide range of hormonal and non-hormonal activities in animals and in vitro, and these activities suggest plausible mechanisms for potential health effects in human subjects consuming phyto-oestrogen-rich diets. In addition, experimental and epidemiological data are available supporting the concept that phyto-oestrogen-rich diets exert physiological effects in vivo; however, their relative importance to human health remains to be elucidated. Our understanding of factors involved in their absorption and metabolism, including the role of intestinal microflora, is limited, and these factors together with dose-related effects may well be important in determining clinical efficacy.