The modification of ageing by nutritional intervention is well recognised. Post-weaning diet restriction is the only widely reproducible method to slow ageing, but the effects of prenatal and preweaning diet restriction have been less well characterised. There is some evidence that diet restriction instituted in utero or shortly after birth may have an opposite effect and be associated with increased ageing, and recent work suggests that it may shorten lifespan. Interest in this area has been rekindled by the growing body of epidemiological evidence showing that a number of age-related diseases are associated with poor growth and inadequate nutrition in early life. The relevance of this association to structural and functional ageing changes in different systems is now being considered. Work on musculo-skeletal ageing has demonstrated that loss of muscle strength and bone mass is greater in individuals who did not grow well in early life, and a range of studies suggests that maternal, developmental and nutritional factors are important. The underlying mechanisms remain speculative, and it remains to be determined whether they are system-specific or universal throughout the body. A new cohort of subjects aged between 60 and 70 years is being established to investigate how genetic factors interact with growth and nutritional influences to programme musculo-skeletal ageing in later life.

Many experiments have shown that foraging animals are sensitive to the riskiness, or variance, associated with alternative food sources. For example, when offered a choice of a constant feeding option that always offers three seeds, and a risky option that offers either no seeds or six seeds with equal probability, most animals tested will be either risk-averse or risk-prone, preferring either the fixed or variable option respectively. Whether animals are risk-averse or risk-prone appears to depend on a range of factors, including the energetic status of the forager, the type of variance associated with the feeding options and even the number of feeding options between which the animal is choosing. These behavioural phenomena have attracted much theoretical interest, and a range of different explanations have been suggested, some based on a consideration of the psychological mechanisms involved in decision making, and others on a consideration of the Darwinian fitness consequences of risk-averse or risk-prone behaviour for the forager. A brief review of the recent literature on risk-sensitive foraging will be presented, focusing on results from the two experimental systems with which I have been involved: wild rufous hummingbirds (Selasphorus rufus) foraging on artificial flowers; European starlings (Sturnus vulgaris) foraging in operant boxes in the laboratory. It will be argued that to understand the foraging decisions of animals account needs to be taken of both the psychological mechanisms underlying decision-making and the fitness consequences of different decisions for the forager.

When talented, motivated and highly trained athletes meet for competition the margin between victory and defeat is usually small. When everything else is equal, nutrition can make the difference between winning and losing. Although the primary concern of many athletes is to supplement the diet with protein, vitamins and minerals, and a range of more exotic compounds, key dietary issues are often neglected. Athletes must establish their nutritional goals, and must also be able to translate them into dietary strategies that will meet these goals. Athletes are often concerned with dietary manipulations in the period around competition, but the main role of nutrition may be to support consistent intensive training which will lead to improved performance. Meeting energy demand and maintaining body mass and body fat at appropriate levels are key goals. An adequate intake of carbohydrate is crucial for maintaining muscle glycogen stores during hard training, but the types of food and the timing of intake are also important. Protein ingestion may stimulate muscle protein synthesis in the post-exercise period, promoting the process of adaptation in the muscles. Restoration of fluid and electrolyte balance after exercise is essential. If energy intake is high and a varied diet is consumed, supplementation of the diet with vitamins and minerals is not warranted, unless a specific deficiency is identified. Specific strategies before competition may be necessary, but this requirement depends on the demands of the sport. Generally, it is important to ensure high pre-competition glycogen stores and to maintain fluid balance. There is limited evidence to support the use of dietary supplements, but some, including perhaps creatine and caffeine, may be beneficial.

Present-day human eating behaviour in industrialised society is characterised by the consumption of high-energy-density diets and often unstructured feeding patterns, largely uncoupled from seasonal cycles of food availability. Broadly similar patterns of feeding are found among advantaged groups in economically-emerging and developing nations. Such patterns of feeding are consistent with the evolutionary ecological understanding of feeding behaviour of hominids ancestral to humans, in that human feeding adaptations are likely to have arisen in the context of resource seasonality in which diet choice for energy-dense and palatable foods would have been selected by way of foraging strategies for the maximisation of energy intake. One hallmark trait of human feeding behaviour, complex control of food availability, emerged with Homo erectus (19 × 106-200 000 years ago), who carried out this process by either increased meat eating or by cooking, or both. Another key trait of human eating behaviour is the symbolic use of food, which emerged with modern Homo sapiens (100 000 years ago to the present) between 25 000 and 12 000 years ago. From this and subsequent social and economic transformations, including the origins of agriculture, humans have come to use food in increasingly elaborate symbolic ways, such that human eating has become increasingly structured socially and culturally in many different ways.

Dietary changes can be difficult to effect both at an individual and at a population level, and even when changes do occur they are often far slower and less pronounced than might be expected. Three possible reason for this situation will be considered: the complexity of food choice and competing influences, attitudinal ambivalence and optimistic bias. Food choice is influenced by a large number of factors, not only health considerations, and therefore it is not surprising that interventions based primarily on health concerns have been ineffective. Another concern is that people do not always have clear-cut attitudes, but rather can be ambivalent about foods and about healthy eating, and this factor might impact on the translation of beliets and attitudes into behaviour. A third possible reason is optimistic bias, where individuals believe themselves to be at less risk from various hazards than is the average person. This effect has been demonstrated for nutritional risks, and this factor might lead people to take less note of health education messages. The stages-of-change model from health psychology has been proposed as a method for improving the effectiveness of behaviour change interventions. However, there are a number of problems in transferring such a model from smoking, where it was originally developed, to dietary behaviours, including the lack of clear-cut specific behaviours and behaviour change targets in the dietary field.

The present paper presents a non-technical overview of contemporary developments in food supply, as seen from the standpoint of economic adjustment. The historical concerns over availability and price of food have now passed in the UK, and agriculture is no longer dominantly driven by the supply-side forces of new farming technology and the stimulus of support policies. As a now demand-driven sector of the economy, it is the developing diversity of consumer food preferences that will increasingly determine the adjustment path of agricultural production. Those demands seek distinctive elements of food value, many of which are entirely created and delivered by industries beyond the farm gate. However, many of the quality characteristics of food that consumers increasingly seek are associated explicitly with what takes place on farms and how crop and livestock husbandry is conducted. In responding to these demand preferences many farmers will shift from being merely raw material producers to becoming genuine producers of food, or capturing more of the final value of the products consumed. As a result a dual structure within farming will develop, with a ‘quality agriculture’ becoming increasingly differentiated from a ‘commodity agriculture’ as two distinct strategies for farm business survival.

A wide variety of plant-derived compounds, including the polyphenolic flavonoids, is present in the human diet or is consumed for medicinal reasons. Epidemiological and animal studies tend to suggest a protective effect of flavonoids against cardiovascular diseases and some types of cancer. Although flavonoids have been studied for about 50 years, the cellular mechanisms involved in their biological activity are still largely unknown. Antioxidant properties of the flavonoids have been postulated as a mechanism for putative protective effect against cardiovascular disease. Nevertheless, these properties alone are not sufficient to explain the anti-carcinogenic potential of these polyphenols. The mechanisms by which the molecules interact with cells or are absorbed by them are very important for determining the intracellular concentration and distribution of the metabolites to internal organs. With the exception of the cells lining the gastrointestinal tract, all other cells in the body are only exposed to flavonoid metabolites and degradation products. No previous studies have addressed this aspect of cellular exposure, except for some methylated metabolites. Within the last decade, reports on flavonoid activities have been largely associated with enzyme inhibition and anti-proliferative activity. From our recent work on the human colon cancer cell line HT29 and comparison with published studies, structure–function relationships demonstrate that antioxidant, enzyme inhibitor or anti-proliferative activities are dependent on particular structure motifs. The present review also presents a summary of mechanistic data on a few selected compounds.

Both jurisdictions of Ireland have high rates of chronic degenerative diseases, particularly of the cardiovascular system, and Irish migrants have worse health profiles, often lasting at least two generations. The influence of socio-demographic variation over the life course, and what role diet plays, has not been well researched in epidemiological terms. There is a long history of an unusual Irish diet. Estimated dietary fat intake (% total energy intake) in 1863 was only 9, but had reached 30 in 1948 and 34 in 1999. Conversely, carbohydrate intake has fallen steadily over 150 years. From 1948 onwards household budget survey data illustrate patterns of increasing urbanisation and socio-economic gradients in food availability. The National Survey of Lifestyles, Attitudes and Nutrition, (n 6539, 622 % response rate) provides clear evidence of inverse social-class gradients in intake of fruit and vegetables and dairy products and in reported patterns of healthy eating. Median carbohydrate and vitamin C levels are higher among social classes 1-2 and mean saturated fat intake is lower. International comparisons indicate a continuing, if narrowing, north-south gradient across Europe. Data from the Boston-Ireland study suggest a crossover in both dietary intake patterns and risk of heart disease in Ireland and the USA in the 1970s. Contemporary comparative data of middle-aged Irish and American women demonstrate patterns of diet intake and inactivity consistent with the modern epidemic of obesity and non-insulin-dependent diabetes. Thus, dietary variations within and between countries and over time are consistent with chronic disease patterns in contemporary Ireland.

The search for the causes of CHD has been guided by a `destructive' model, which proposes that influences acting in adult life, such as smoking, obesity or high saturated fat intakes, lead to an acceleration of age-related destructive processes, including a rise in blood pressure and the formation of atheroma. One explanation for the failure of the model to account for, or indeed to prevent rising epidemics of CHD, is that individuals are heterogeneous in their responses to such influences. This heterogeneity in response is linked to different paths of early growth. The recent discovery that individuals who develop CHD grew differently from other individuals during fetal life and in childhood has led to a new `developmental' model for the disease. Reduced fetal growth followed by poor growth in infancy leads to an increased risk of development of CHD, and its associated conditions, stroke, hypertension and impaired glucose tolerance. These effects are compounded by accelerated weight gain, which may represent 'compensatory growth' in childhood.

De novo lipogenesis is the biological process by which C2 precursors of acetyl-CoA are synthesized into fatty acids. In human subjects consuming diets higher in fat (>30 % energy), lipogenesis is down regulated and extremely low; typically < 10 % of the fatty acids secreted by the liver. This percentage will increase when dietary fat is reduced and replaced by carbohydrate, although the extent of carbohydrate-induced lipogenesis is dependent on the type of carbohydrate (monosaccharide v. polysaccharide) and the form in which the carbohydrate is fed (liquid meals, solid less-processed food). Clearly, massive overconsumption of carbohydrate can also increase lipogenesis. A second related phenomenon that occurs when dietary fat is reduced is hypertriacylglycerolaemia. This rise in blood triacylglycerol concentration could be due to increased de novo lipogenesis or to reduced clearance of lipid from the blood. The present paper will review the metabolic mechanisms leading to the elevations in blood triacylglycerol concentration that occur with dietary fat reduction. Studies considered will be those investigating fatty acid synthesis in subjects chronically fed low-fat high-carbohydrate diets and studies in which data were obtained in both the fasted and fed states. Also summarized will be data from subjects who had consumed diets of different carbohydrate types, as well as the most recent data from postprandial studies investigating factors that affect the magnitude of the rise in blood lipids following a meal. Given the changing availability of carbohydrate in the food supply, it will be important to understand how the balance of fat and carbohydrate in the diet influences lipogenesis, and the relative contribution of the process of de novo lipogenesis to the escalating incidence of obesity observed around the world.

Members of the nuclear steroid hormone superfamily mediate essential physiological functions. Steroid hormone receptors (SHR) act directly on DNA, regulate the synthesis of their target genes and are usually activated by ligand binding. Both endogenous and exogenous compounds and their metabolites may act as activators of SHR and disruptors of endocrine, cellular and lipid homeostasis. The endogenous ligands are generally steroids such as 17β-oestradiol, androgens, progesterone and pregnenolone. The exogenous compounds are usually delivered through the diet and include non-steroidal ligands. Examples of such ligands include isoflavanoids or phyto-oestrogens, and food contaminants such as exogenous oestrogens from hormone-treated cattle, pesticides, polychlorinated biphenyls and plasticisers. Certain drugs are also ligands; so nuclear receptors are also important drug targets for intervention in disease processes. The present review summarises recent reports on ligand-activated SHR that describe the selective regulation of a tightly-controlled cross-talking network involving exchange of ligands, and the control of major classes of cytochrome P450 (CYP) isoforms which metabolise many bioactive exogenous compounds. Many CYP have broad substrate activity and appear to be integrated into a coordinated metabolic pathway, such that whilst some receptors are ligand specific, other sensors may have a broader specificity and low ligand affinity to monitor aggregate levels of inducers. They can then trigger production of metabolising enzymes to defend against possible toxic nutrients and xenobiotic compounds. The influence of dietary intakes of nutrients and non-nutrients on the human oestrogen receptors (α and β), the aryl hydrocarbon receptor, the pregnane X receptor, the constitutive androstane receptor, and the peroxisome proliferator-activated receptors (α and γ), can be examined by utilising computer-generated molecular models of the ligand–receptor interaction, based on information generated from crystallographic data and sequence homology. In relation to experimental and observed data, molecular modelling can provide a scientifically sound perspective on the potential risk and benefits to human health from dietary exposure to hormone-mimicking chemicals, providing a useful tool in drug development and in a situation of considerable public concern.

Crohn’s disease is a modern Western disease characterised by transmural inflammation of the gastrointestinal tract. It is of unknown aetiology, but evidence suggests that it results from a combination of genetic predisposition and environmental factors. Bacterial-sized microparticles (0·1–1·0 µm) are potent adjuvants in model antigen-mediated immune responses and are increasingly associated with disease. Microparticles of TiO2 and aluminosilicate accumulate in macrophages of human gut-associated lymphoid tissue where the earliest signs of lesions in Crohn’s disease are observed. Dietary microparticles are of endogenous or exogenous origin. Endogenous microparticles dominate and are calcium phosphate (most probably hydroxyapatite), which precipitates in the lumen of the mid-distal gastrointestinal tract due to secretion of Ca and phosphate in the succus entericus. Exogenous dietary microparticles are contaminants (soil and/or dust) and food additives. TiO2, for example, is a food colourant, and aluminosilicates are anti-caking agents, although some aluminosilicates occur as natural contaminants. Food additives alone account for ingestion of approximately 1012 particles/person per d. Possible mechanisms for the role of exogenous and endogenous dietary microparticles in promoting toleragenic or immune responses of gastrointestinal mucosal phagocytosis are discussed. In a double-blind randomised pilot study we have shown that a diet low in Ca and exogenous microparticles appears to alleviate the symptoms of ileal Crohn’s disease, with a significant (P = 0·002) improvement in the Crohn’s disease activity index. A multi-centre trial and further mechanistic studies at the cellular level are underway.

There is a growing database that has evaluated the effects of varying amounts of total fat on risk factors for cardiovascular disease, diabetes and overweight and obesity. The evidence clearly suggests that extremes in dietary fat should be avoided, and instead a diet moderate in total fat (25–35 % energy) is preferable for the majority of individuals. Moreover, we now appreciate the importance of individualizing dietary fat recommendations within this range of total fat. With respect to cardiovascular disease, a diet higher in total fat (30–35 % energy) affects the lipid and lipoprotein risk profile more favourably than a lower-fat diet; this is also the case for individuals with diabetes, with the added benefit of better glycaemic control. Dietary fibre (≧25g/d) attenuates and even prevents the potentially adverse lipid and lipoprotein effects of a lower-fat diet. With respect to weight control, a moderate-fat diet can be as, or even more, effective than a lower-fat diet, because of advantages with long-term adherence and potentially favourable effects on lipids and lipoproteins. Thus, there is now a convincing scientific basis to advocate a diet moderate in total fat for the majority of individuals. Implicit to this position is that unsaturated fat has numerous beneficial health effects. However, because fat is energy dense, moderation in fat intake is essential for weight control. Consequently, a simple message to convey is to avoid diets that are very low and very high in fat. Moreover, within the range of a moderate-fat diet it is still important to individualize the total fat prescription. Nonetheless, the guiding principle is that moderation in total fat is the defining benchmark for a contemporary diet that reduces risk of chronic disease.

Glucose intolerance represents a spectrum of abnormalities, including impaired fasting glucose, impaired glucose tolerance and type 2 diabetes. It is a major public health challenge worldwide, with rapidly increasing prevalence rates in both developed and developing countries. This global epidemic of diabetes is largely driven by the globalisation of Western culture and lifestyles. Specifically, there is now evidence from large-scale observational studies, and from intervention studies, of powerful synergistic interactions between diet, obesity, exercise, smoking and alcohol in the development of glucose intolerance. It is estimated that > 90 % of cases of type 2 diabetes in the population could be prevented with the adoption of a prudent diet (high in cereal fibre and polyunsaturated fatty acids and low in trans-fatty acids and glycaemic load), avoidance of overweight and obesity (BMI < 25 kg/m2), engagement in moderate to vigorous physical activity for at least 05 h/d, non-smoking and moderate alcohol consumption. These findings are biologically plausible and have major public health implications. They form the basis for a clear, simple and coherent message for health promotion and public policy. However, to make progress on these issues health will need to be placed at the centre of public policy and relevant vested interests tackled, notably in the food, entertainment, tobacco and automobile industries.

The role of high-fat diets in weight gain and obesity is assessed by evidence-based principles. Four meta-analyses of weight change occurring on ad libitum low-fat diets in intervention trials consistently demonstrate a highly significant weight loss of 3–4 kg in normal-weight and overweight subjects (P< 0·001). The analyses also find a dose-response relationship, i.e. the reduction in percentage energy as fat is positively associated with weight loss. Weight loss is also positively related to initial weight; a 10 % reduction in dietary fat is predicted to produce a 4–5 kg weight loss in an individual with a BMI of 30kg/m2. The non-fat macronutrient composition of the diet is also important. Whereas the glycaemic index of the carbohydrate may play a role for cardiovascular risk factors, there is so far no evidence that low-glycaemic index foods facilitate weight control. In contrast, intervention studies show that sugar in drinks is more likely to produce weight gain than solid sugar in foods. Although the evidence is weak, alcoholic beverages promote a positive energy balance, and wine may be more obesity-promoting than beer. Protein is more satiating and fhermogenic than carbohydrates, and one intervention study has shown that an ad libitum low-fat diet where carbohydrate was replaced by protein produced more weight loss after 6 months (8·1 v. 5·9 kg). The evidence linking particular fatty acids to body fatness is weak. If anything, monounsaturated fat may be more fattening than polyunsaturated and saturated fats, and no ad libitum dietary intervention study has shown that a normal-fat high-monounsaturated fatty acid diet is equivalent or superior to a low-fat diet in the prevention of weight gain and obesity. The evidence strongly supports the low-fat diet as the optimal choice for the prevention of weight gain and obesity, while the use of a normal-fat high-monounsaturated fatty acid diet is unsubstantiated.

Chronic infection with HIV type 1 is associated with alterations in macronutrient metabolism, specifically elevated plasma lipids, glucose and reduced insulin sensitivity. These alterations are most severe in patients at the later stages of AIDS, indicating a relationship with disease progression. Recently, a metabolic syndrome, termed lipodystrophy, has been described in successfully-treated HIV patients in whom the altered macronutrient metabolism of HIV infection appears to be amplified markedly, with concurrent alterations in adipose tissue patterning. This syndrome presents a paradox, as before the development of highly-active antiretroviral therapy (HAART) the most severe perturbations in metabolism were observed in the sickest patients. Now, the patients that respond well to therapy are showing metabolic perturbations much greater than those seen before. The implications of this syndrome are that, whilst life expectancy may be increased by reducing viral load, there are concomitant increases in the risk of cardiovascular disease, diabetes and pancreatitis within this patient population. The aetiology of the syndrome remains unclear. In a collaborative trial with the Chelsea and Westminster Hospital in London we have used stable-isotope-labelled fatty acids to examine the hypothesis that treatment with HAART causes a delayed clearance of dietary lipid from the circulation, resulting in the retention of lipid within plasma and the downstream changes in insulin and glucose homeostasis. This hypothesis would indicate a role for low-fat diets, exercise and drugs that reduce plasma lipid or insulin resistance, in modulating the response to antiretroviral therapy in HIV infection.

Socially-and culturally-patterned differences in food habits exist both between and within European populations. Daily individual food availability data, collected through the national household budget surveys (HBS) and harmonized in the context of the Data Food Networking (DAFNE) project, were used to assess disparities in food habits of seven European populations and to evaluate dietary changes within a 10-year interval. The availability of selected food items was further estimated according to the educational level of the household head and, based only on the Greek HBS data, according to quintiles of the household's food purchasing capacity. Results for overall food availability support the north-south differentiation in food habits. Generally, the availability of most food items, including foods such as vegetable fats, animal lipids and sugar products, has decreased over the 10 years. Households in which the head was in the higher education categories reported lower availability for most food items, with the exception of low-fat milk, fresh fruit, animal lipids and soft drinks; the latter showing a sharp increase even within southern European households. The household's food purchasing capacity can be used as an indicator of socio-economic status, with higher values being associated with lower status. Greek households of lower social class follow a healthier diet in terms of greater availability of vegetable oils, fresh vegetables, legumes, fish and seafood. Data from the DAFNE databank may serve as a tool for identifying and quantifying variation in food habits in Europe, as well as for providing information on the socio-economic determinants of food preferences.

Periodontal disease is a common chronic adult condition. The bacterium Porphyromonas gingivalis has been implicated in the aetiology of this disease, which causes destruction of the connective tissue and bone around the root area of the tooth. It has been observed that invading P. gingivalis bacteria trigger the release of cytokines such as interleukin 8 and tumour necrosis factor α, leading to elevated numbers and activity of polymorphonucleocytes (PMN). As a result of stimulation by bacterial antigens, PMN produce the reactive oxygen species (ROS) superoxide via the respiratory burst as part of the host response to infection. Patients with periodontal disease display increased PMN number and activity. It has been suggested that this proliferation results in a high degree of ROS release, culminating in heightened oxidative damage to gingival tissue, periodontal ligament and alveolar bone. Antioxidant constituents in plasma have been well-documented, being chiefly ascorbate, albumin and urate, and these are known to display sensitivity to dietary antioxidant intakes. The concentration of antioxidants in saliva does not appear to mirror those of plasma. The extent of dietary influence upon salivary antioxidant status is unclear. Urate is the predominant salivary antioxidant, with albumin and ascorbate providing minor contributions. Previous research has found reduced salivary antioxidant activity in patients suffering from periodontal disease. An improved understanding of the role antioxidants play in periodontitis, and the influence of nutrition on antioxidant status, may lead to a possible nutritional strategy for the treatment of periodontal disease.

Development of effective intervention strategies to meet the needs of people with ethnic minority origins is dependent on two factors: an understanding of the modifiable risk factors which can form the basis of intervention; an understanding of the relevant health behaviours so that appropriate strategies can be designed. The present paper briefly reviews the evidence concerning the part that nutritional and dietary factors play in the aetiology of the observed patterns of disease in these groups and the limitations of the data as a basis for intervention. Consideration is also given to the available information concerning factors influencing health behaviour (particularly eating behaviour) and the applicability of commonly-used models of behaviour change to people of ethnic minority origin. Finally, the results of nutrition intervention programmes will be examined with a view to identifying lessons for the future.

As a result of the increasing consumer demand for minimally-processed fresh-like food products with high sensory and nutritional qualities, there is a growing interest in non-thermal processes for food processing and preservation. Key advanced technologies such as high-pressure processing, pulsed electric fields, dense gases and ultrasound are being applied to develop gentle but targeted processes to further improve the quality and safety of processed foods. These technologies also offer the potential for improving existing processes as well as for developing new process options. Furthermore, by adding new process dimensions (such as hydrostatic pressure, electric fields, ultrasonics, supercritical CO2) to the conventional process variables of temperature and time, they facilitate enlargement of the availability of unit operations. These operations might be applied effectively in unique combination processes, or as subsequent processing tools in more-targeted and subsequently less-intensive processes for food preservation and modification than the currently-applied processes.