Waterlow's (1981) Sixth Boyd Orr Lecture on a ‘crisis of identity for nutrition’ stimulated the Nutrition Society's drive to professionalisation. Twenty-five years on, the Society begins a new stage; first, towards an independent voluntary regulator, and then towards statutory regulation. It is timely to reflect on progress and identify the remaining challenges. The Society has made impressive progress as a voluntary regulator since 1991 when the Insitute of Biology opened a register in cooperation with the Institute of Food Science and Technology and the Nutrition Society; the present register is 2·75-fold larger. The Society has specialist standards for course accreditation that enable graduates to apply for direct entry to the register, having met standards of competency in nutrition or public health nutrition. A code of ethics and a statement of professional conduct underpin a functioning system for oversight and governance that protects the public, the hallmark of all professions. Registered nutritionists lay easy claim to a unique science basis for their profession. A scheme for continuing professional development (CPD) started in July 2006, 1 year before a sample audit starts to show the link between CPD and re-registration. The scheme will be piloted in the first year. The critical challenge is the issue of identity. Waterlow (1981) stated that professional registration must lead explicitly and formally to a specific vocation, an occupation that provides services that society requires and one that contributes to the well-being and health of all. The present time may be the last and best chance for nutritionists, as nutrition has a higher priority for government in the UK than ever before. The Society has begun to help in strategic public health workforce planning and development; new and still plastic, it is the ideal locus from which a discipline and a profession can emerge. The CPD scheme will work if it helps nutritionists meet their own needs; more mutual cooperation and consensus about real world standards of performance are needed. Nutritionists need to show how they actually contribute to national health and/or wealth. Then, sustained resources can be advocated for and the support of the voting public and legislators secured, without which it will not be possible to get the legal protection that is desirable for the profession.

Complementary neurophysiological recordings in rhesus macaques (Macaca mulatta) and functional neuroimaging in human subjects show that the primary taste cortex in the rostral insula and adjoining frontal operculum provides separate and combined representations of the taste, temperature and texture (including viscosity and fat texture) of food in the mouth independently of hunger and thus of reward value and pleasantness. One synapse on, in the orbitofrontal cortex, these sensory inputs are for some neurons combined by learning with olfactory and visual inputs. Different neurons respond to different combinations, providing a rich representation of the sensory properties of food. In the orbitofrontal cortex feeding to satiety with one food decreases the responses of these neurons to that food, but not to other foods, showing that sensory-specific satiety is computed in the primate (including the human) orbitofrontal cortex. Consistently, activation of parts of the human orbitofrontal cortex correlates with subjective ratings of the pleasantness of the taste and smell of food. Cognitive factors, such as a word label presented with an odour, influence the pleasantness of the odour, and the activation produced by the odour in the orbitofrontal cortex. Food intake is thus controlled by building a multimodal representation of the sensory properties of food in the orbitofrontal cortex and gating this representation by satiety signals to produce a representation of the pleasantness or reward value of food that drives food intake. Factors that lead this system to become unbalanced and contribute to overeating and obesity are described.

The newborn receives, via the placenta, maternal IgG antibodies against the microbes present in its surroundings, but such antibodies have a pro-inflammatory action, initiating the complement system and phagocytes. Although the host defence mechanisms of the neonate that involve inflammatory reactivity are somewhat inefficient, this defence system can still have catabolic effects. Breast-feeding compensates for this relative inefficiency of host defence in the neonate by providing considerable amounts of secretory IgA antibodies directed particularly against the microbial flora of the mother and her environment. These antibodies bind the microbes that are appearing on the infant's mucosal membranes, preventing activation of the pro-inflammatory defence. The major milk protein lactoferrin can destroy microbes and reduce inflammatory responses. The non-absorbed milk oligosaccharides block attachment of microbes to the infant's mucosae, preventing infections. The milk may contain anti-secretory factor, which is anti-inflammatory, preventing mastitis in mothers and diarrhoea in infants. Numerous additional factors in the milk are of unknown function, although IL-7 is linked to the larger size of the thymus and the enhanced development of intestinal Tγδ lymphocytes in breast-fed compared with non-breast-fed infants. Several additional components in the milk may help to explain why breast-feeding can reduce infant mortality, protecting against neonatal septicaemia and meningitis. It is therefore important to start breast-feeding immediately. Protection is also apparent against diarrhoea, respiratory infections and otitis media. There may be protection against urinary tract infections and necrotizing enterocolitis, and possibly also against allergy and certain other immunological diseases, and tumours. In conclusion, breast-feeding provides a very broad multifactorial anti-inflammatory defence for the infant.

Human milk provides all the dietary essential fatty acids, linoleic acid (LA; 18:2n-6) and α-linolenic acid (18:3n-3), as well as their longer-chain more-unsaturated metabolites, including arachidonic acid (20:4n-6) and DHA (22:6n-3) to support the growth and development of the breast-fed infant. Human milk levels of LA have increased in Westernized nations from mean levels (g/100 g total fatty acids) of 6 to 12–16 over the last century, paralleling the increase in dietary intake of LA-rich vegetable oils. DHA levels (g/100 g total milk fatty acids) vary from <0·1 to >1% and are lowest in countries in which the intake of DHA from fish and other animal tissue lipids is low. The role of DHA in infant nutrition is of particular importance because DHA is accumulated specifically in the membrane lipids of the brain and retina, where it is important to visual and neural function. An important question is the extent to which many human diets that contain low amounts of n-3 fatty acids may compromise human development. The present paper reviews current knowledge on maternal diet and human milk fatty acids, the implications of maternal diet as the only source of essential fatty acids for infant development both before and after birth, and recent studies addressing the maternal intakes and milk DHA levels associated with risk of low infant neural system maturation.

Cravings are hedonic responses to food, characterised by their intensity and their specificity. Food cravings are extremely common, reported by the majority of young adults. They are closely associated with liking but not synonymous with increased intake. Structured interviews and prospective incident accounts of food cravings have succeeded in revealing a richness of information about their character, their antecedents and their consequences. In addition, laboratory investigations are adding to what is being learned from field and clinical studies. Taking dieting as an example of an assumed influence on food craving, the outcomes of cross-sectional studies are mixed and unconvincing. Prospective and experimental research shows a clearer relationship. Dieting or restrained eating generally increase the likelihood of food craving while fasting makes craving, like hunger, diminish. Attempted restriction or deprivation of a particular food is associated with an increase in craving for the unavailable food. This relationship suggests a variety of underlying cognitive, conditioning and emotional processes, of which ironic cognitive processes, conditioned cue reactivity and dysphoric mood are prominent. Food cravings may also be self-attributions, accounting for why a highly-palatable but self-restricted food is (over-)consumed. Overall, the popularised account of cravings as elicited by specific nutritional need is having to give way to a more subtle and complex appreciation of human eating behaviour.

Human food intake is driven by necessity, but modern industrialized societies are characterized by food surfeit and an increasingly ‘obesogenic’ environment. This environment tends to discourage energy expenditure and to facilitate energy intake. The amount eaten in any given eating episode depends less on internal need state and more on environmental contextual factors such as the availability of highly-palatable energy-dense foods. In addition, the process of satiation can easily be disrupted by the introduction within a meal of different foods (variety effect), the presence of others (social context) and competing tasks (distraction). Properties of ingestants such as alcohol promote food intake and characteristics of individuals make them more or less susceptible to situational cues to overeat. In the present review the role of each of these environmental factors in promoting overconsumption are considered and the extent to which these factors might contribute to long-term weight regulation is discussed.

Rodent models of diet-induced obesity (DIO) mimic common human obesity more accurately than obese single-gene mutation lines, such as the ob/ob mouse. Sprague-Dawley rats sourced in the UK develop obesity when fed a high-energy diet, but susceptibility to DIO is normally distributed, as might be anticipated for a polygenic trait in an outbred population, in contrast to reports in the literature using ostensibly the same strain of rats sourced in the USA. Nevertheless, the responses of these rats to solid and liquid obesogenic diets are very similar to those reported elsewhere, and this model of DIO has much to commend it as a vehicle for the mechanistic study of susceptibility to DIO, development and reversal of obesity on solid and liquid diets and the response of peripheral and central energy balance systems to the development of obesity and to the obesogenic diets themselves. In general, hypothalamic energy-balance-related systems respond to obesogenic diets and developing obesity with activity changes that appear designed to counter the further development of the obese state. However, these hypothalamic changes are apparently unable to maintain body weight and composition within normal limits, suggesting that attributes of the obesogenic diets either evade the normal regulatory systems and/or engage with reward pathways that override the homeostatic systems. Since diets are a risk factor in the development of obesity, it will be important to establish how obesogenic diets interact with energy-balance pathways and whether there is potential for diets to be manipulated with therapeutic benefit.

The prevalence of the metabolic syndrome (MetS), CVD and type 2 diabetes (T2D) is known to be higher in populations from the Indian subcontinent compared with the general UK population. While identification of this increased risk is crucial to allow for effective treatment, there is controversy over the applicability of diagnostic criteria, and particularly measures of adiposity in ethnic minorities. Diagnostic cut-offs for BMI and waist circumference have been largely derived from predominantly white Caucasian populations and, therefore, have been inappropriate and not transferable to Asian groups. Many Asian populations, particularly South Asians, have a higher total and central adiposity for a similar body weight compared with matched Caucasians and greater CVD risk associated with a lower BMI. Although the causes of CVD and T2D are multi-factorial, diet is thought to make a substantial contribution to the development of these diseases. Low dietary intakes and tissue levels of long-chain (LC) n-3 PUFA in South Asian populations have been linked to high-risk abnormalities in the MetS. Conversely, increasing the dietary intake of LC n-3 PUFA in South Asians has proved an effective strategy for correcting such abnormalities as dyslipidaemia in the MetS. Appropriate diagnostic criteria that include a modified definition of adiposity must be in place to facilitate the early detection and thus targeted treatment of increased risk in ethnic minorities.

The human colonic microflora has a central role in health and disease, being unique in its complexity and range of functions. As such, dietary modulation is important for improved gut health, especially during the highly-sensitive stage of infancy. Diet can affect the composition of the gut microflora through the availability of different substrates for bacterial fermentation. Differences in gut microflora composition and incidence of infection exist between breast-fed and formula-fed infants, with the former thought to have improved protection. Historically, this improvement has been believed to be a result of the higher presence of reportedly-beneficial genera such as the bifidobacteria. As such, functional food ingredients such as prebiotics and probiotics could effect a beneficial modification in the composition and activities of gut microflora of infants by increasing positive flora components. The prebiotic approach aims to increase resident bacteria that are considered to be beneficial for human health, e.g. bifidobacteria and lactobacilli, while probiotics advocates the use of the live micro-organisms themselves in the diet. Both approaches have found their way into infant formula feeds and aim to more closely simulate the gut microbiota composition seen during breast-feeding.

More than 70 years ago the glucostatic, lipostatic and aminostatic hypotheses proposed that the central nervous system sensed circulating levels of different metabolites, changing feeding behaviour in response to the levels of those molecules. In the last 20 years the rapid increase in obesity and associated pathologies in developed countries has involved a substantial increase in the knowledge of the physiological and molecular mechanism regulating body mass. This effort has resulted in the recent discovery of new peripheral signals, such as leptin and ghrelin, as well as new neuropeptides, such as orexins, involved in body-weight homeostasis. The present review summarises research into energy balance, starting from the original classical hypotheses proposing metabolite sensing, through peripheral tissue–brain interactions and coming full circle to the recently-discovered role of hypothalamic fatty acid synthase in feeding regulation. Understanding these molecular mechanisms will provide new pharmacological targets for the treatment of obesity and appetite disorders.

Fe deficiency is a common nutritional disorder during infancy, particularly in low-income countries. The Fe status of a breast-fed infant is strongly influenced by the body Fe content at birth, which is determined by factors that operate before birth (maternal Fe status before and during pregnancy; infant gestational age and birth weight) and at the time of delivery (the timing of umbilical cord clamping). Delaying the clamping of the umbilical cord for 2 min can increase body Fe content by approximately 33% (75 mg), and results in greater Fe stores at 6 months of age. After birth, male gender and a rapid rate of weight gain are associated with lower Fe status. During the first half of infancy dietary Fe requirements depend on Fe stores at birth. For an exclusively-breast-fed full-term normal-birth-weight infant with delayed umbilical cord clamping, whose mother had adequate Fe status during pregnancy, the Fe provided from stores and breast milk is sufficient for ≥6 months, but before this time higher-risk infants may become Fe deficient. Fe supplementation can be beneficial for high-risk infants, but can have adverse effects on growth and morbidity of Fe-replete infants. After 6 months most breast-fed infants will require complementary foods that are rich in Fe.

There is now compelling evidence that growth patterns in early life are associated with risk of the metabolic syndrome in adulthood, although the relative importance of prenatal v. postnatal growth for such associations remains controversial. Body composition may play a key role in the ‘programming’ of such diseases, through itself being programmed by early growth, and perhaps also by being a mediator of the programming process. Early studies reporting positive associations between birth weight and adult BMI suggested a tendency for large babies to become obese adults. Such findings appeared contradictory to the many studies linking low birth weight with increased risk of the metabolic syndrome. Recent studies now indicate that birth weight is strongly predictive of later lean mass, and has a much weaker association with later fatness. Studies that link low birth weight with a more central adipose distribution in later life remain controversial, and require confirmation using more sophisticated methodologies. Findings for infant growth rate appear population-specific, with infant weight gain predicting subsequent lean mass in developing countries, but predicting subsequent fat mass and obesity in industrialised populations. Further studies are required on this issue, to ensure that appropriate public health policies are recommended for countries across the range of economic development. Although the links between early growth and later disease risk implicate early-life nutrition, either in utero or during infancy, few prospective studies have explored the influence of early diet on later body composition. Many studies have associated breast-feeding with a reduced prevalence of obesity categorised by BMI; however, the few studies directly evaluating childhood fatness provide little support for this hypothesis. Recent advances in the ability to measure body composition during the infant period offer a major opportunity to improve the understanding of the nutritional programming of body composition and its contribution, or lack thereof, to subsequent disease risk.

Increasing evidence from lifetime experimental studies in animals and observational and experimental studies in human subjects suggests that pre- and postnatal nutrition programme long-term health. However, key unanswered questions remain on the extent of early-life programming in contemporary European populations, relevant nutritional exposures, critical time periods, mechanisms and the effectiveness of interventions to prevent or reverse programming effects. The EARly Nutrition programming – long-term Efficacy and Safety Trials and integrated epidemiological, genetic, animal, consumer and economic research (EARNEST) consortium brings together a multi-disciplinary team of scientists from European research institutions in an integrated programme of work that includes experimental studies in human subjects, modern prospective observational studies and mechanistic animal work including physiological studies, cell-culture models and molecular techniques. Theme 1 tests early nutritional programming of disease in human subjects, measuring disease markers in childhood and early adulthood in nineteen randomised controlled trials of nutritional interventions in pregnancy and infancy. Theme 2 examines associations between early nutrition and later outcomes in large modern European population-based prospective studies, with detailed measures of diet in pregnancy and early life. Theme 3 uses animal, cellular and molecular techniques to study lifetime effects of early nutrition. Biomedical studies are complemented by studies of the social and economic importance of programming (themes 4 and 5), and themes encouraging integration, communication, training and wealth creation. The project aims to: help formulate policies on the composition and testing of infant foods; improve the nutritional value of infant formulas; identify interventions to prevent and reverse adverse early nutritional programming. In addition, it has the potential to develop new products through industrial partnerships, generate information on the social and economic cost of programming in Europe and help maintain Europe's lead in this critical area of research.

It is now well established that an imbalance or reduction in the maternal diet either through pregnancy and lactation or at defined time points therein can have long-term effects on cardiovascular and metabolic health in the resulting offspring; the exact outcome varying greatly with the period of development or growth targeted. The EARly Nutrition programming – long-term follow up of Efficacy and Safety Trials and integrated epidemiological, genetic, animal, consumer and economic research (EARNEST), or metabolic programming, project aims to determine the primary physiological and molecular mechanisms that cause long-term changes in both cardiovascular function and metabolic homeostasis. Thereafter, it also aims to examine nutritional interventions that could be adopted in order to overcome such complications. The present review summarises some of the more recent findings from a range of nutritional interventions in both small and large animals that are beginning to uncover novel pathways by which long-term health can be determined. These interventions include nutritional manipulations that can increase or decrease blood pressure in the resulting offspring as well as indicating their dissociation from adaptations in the kidney. Particular emphasis will be placed on growth during lactation in conjunction with the extent to which central and peripheral tissue adaptations can act to amplify, or protect, the offspring from later disease when born to nutritionally-manipulated mothers.

Size at birth and patterns of postnatal weight gain have been associated with adult risk for the development of type 2 diabetes in many populations, but the putative pathophysiological link remains unknown. Studies of contemporary populations indicate that rapid infancy weight gain, which may follow fetal growth restriction, is an important risk factor for the development of childhood obesity and insulin resistance. Data from the Avon Longitudinal Study of Pregnancy and Childhood shows that rapid catch-up weight gain can lead to the development of insulin resistance, as early as 1 year of age, in association with increasing accumulation of central abdominal fat mass. In contrast, the disposition index, which reflects the β-cells ability to maintain insulin secretion in the face of increasing insulin resistance, is much more closely related to ponderal index at birth than postnatal catch-up weight gain. Infants with the lowest ponderal index at birth show a reduced disposition index at aged 8 years associated with increases in fasting NEFA levels. The disposition index is also closely related to childhood height gain and insulin-like growth factor-I (IGF-I) levels; reduced insulin secretory capacity being associated with reduced statural growth, and relatively short stature with reduced IGF-I levels at age 8 years. IGF-I may have an important role in the maintenance of β-cell mass, as demonstrated by recent studies of pancreatic β-cell IGF-I receptor knock-out and adult observational studies indicating that low IGF-I levels are predictive of subsequent risk for the development of type 2 diabetes. However, as insulin secretion is an important determinant of IGF-I levels, cause and effect may be difficult to establish. In conclusion, although rapid infancy weight gain and increasing rates of childhood obesity will increase the risk for the development of insulin resistance, prenatal and postnatal determinants of β-cell mass may ultimately be the most important determinants of an individual's ability to maintain insulin secretion in the face of increasing insulin resistance, and thus risk for the development of type 2 diabetes.

Carotenoids and retinoids are groups of nutritionally-relevant compounds present in many foods of plant origin (carotenoids) and animal origin (mainly retinoids). Their levels in human subjects vary depending on the diversity and amount of the individual's nutrient intake. Some carotenoids and retinoids have been investigated for their effects on the immune system both in vitro and in vivo. It has been shown that retinoids have the potential to mediate or induce proliferative and differentiating effects on several immune-competent cells, and various carotenoids are known to be inducers of immune function. The immune-modulating effects of retinoids have been well documented, while the effects of carotenoids on the immune system have not been investigated as extensively, because little is known about their molecular mechanism of action. The present review will mainly focus on the molecular mechanism of action of retinoids and particularly carotenoids, their nutritional origin and intake, their transfer from the maternal diet to the child and their effects or potential effects on the developing immune system.