In the present paper the prevalence of obesity (BMI 30 kg/m2) and current physical activity levels in Irish adults have been evaluated. The prevalence of obesity in Irish adults is currently 18 %, with men at 20 % and women at 16 %. A further 47 % of men and 33 % of women are overweight (BMI 25·0–29·9 kg/m2). Since 1990, obesity has more than doubled in men from 8 % to 20 %, and increased from 13 % to 16 % in women. The highest prevalence of obesity (30 %) was found in women aged 51–64 years. Defined waist circumference action levels identified 48 % of the population who are in need of weight management and who also are at a 1·5–4·5 times increased risk of having at least one cardiovascular disease risk factor. Physical activity levels were low overall. Men were more active in work and recreational pursuits than women, but women were more active in household activities. Walking was the most popular recreational pursuit. However, TV viewing occupied most of the leisure time of men and women. Higher levels of activity were associated with a lower BMI and waist circumference. The results indicate the need for sensitive and individualised strategies to promote physical activity and to achieve a healthy weight status.

The high incidence of obesity in Ireland is of growing concern. The Irish Universities Nutrition Alliance North/South Food Consumption Survey found that 18 % of the population are obese and 39 % overweight. Obesity and overweight increase the risk of developing CHD, type 2 diabetes, hypertension and some forms of cancer. It is well accepted that the best treatment for obesity is a combination of energy intake reduction and regular exercise. Previously, dietary compliance has been shown to improve when monitored on a regular basis. The lengthy delay between clinic visits to the dietitian has been reported by those who failed to lose weight to be the main reason for poor compliance. A weight monitoring clinic was designed to offer those requiring regular support and encouragement the opportunity to monitor their weights on a more regular basis, while waiting for their return visit to the dietitian in the Outpatient Departments. As resources were limited, an efficient use of time was essential. The clinic design was: 1 h/week; eight to fourteen appointments per clinic; weekly or fortnightly visit; return patients only. The clinic was started on a trial basis in June 1999, and was evaluated in December 2000. Referrals were only taken from other dietitians, and each participant was informed in advance of the necessity of having a return Outpatient Department appointment for full dietary review. Forty-eight participants attended more than three times up to and including December 2000 (seven males, forty-one females). The number of clinic visits ranged from three to twenty-eight. Mean weight at start of clinic was 92·94 kg. Of the group attending, 67 % (thirty-two) successfully lost weight and maintained this weight loss. This ranged from 0·1 kg to 23·5 kg. While in total 31 % (fifteen) of attendees had gained weight at December 2000, all attendees, including this fifteen, had lost weight at some point during the clinic. Self-reported reasons given for weight regain included: (1) non-attendance at weight clinic (40 %); (2) Christmas or holidays (13 %); (3) stress related to family, work (13 %); (4) ill-health or medication (13 %). The remaining 20 % reported no reason. Other findings included better compliance with diet and improved overall balance. There was an overall improvement in other dietary-related problems, e.g. reduced cholesterol, improved glycaemic control, reduced blood pressure. The participants attending the clinic reported decreased clothes size and improved self-image and confidence. They were more enthusiastic about dietary compliance, and all attendees expressed their satisfaction with the clinic and the service.

Emphasis on public health and consumer protection, in combination with globalisation of the food market, has created a strong demand for exposure assessments of food chemicals. The food chemicals for which exposure assessments are required include food additives, pesticide residues, environmental contaminants, mycotoxins, novel food ingredients, packaging-material migrants, flavouring substances and nutrients. A wide range of methodologies exists for estimating exposure to food chemicals, and the method chosen for a particular exposure assessment is influenced by the nature of the chemical, the purpose of the assessment and the resources available. Sources of food consumption data currently used in exposure assessments range from food balance sheets to detailed food consumption surveys of individuals and duplicate-diet studies. The fitness-for-purpose of the data must be evaluated in the context of data quality and relevance to the assessment objective. Methods to combine the food consumption data with chemical concentration data may be deterministic or probabilistic. Deterministic methods estimate intakes of food chemicals that may occur in a population, but probabilistic methods provide the advantage of estimating the probability with which different levels of intake will occur. Probabilistic analysis permits the exposure assessor to model the variability (true heterogeneity) and uncertainty (lack of knowledge) that may exist in the exposure variables, including food consumption data, and thus to examine the full distribution of possible resulting exposures. Challenges for probabilistic modelling include the selection of appropriate modes of inputting food consumption data into the models.

Consumer concern regarding possible adverse health effects of foods produced using intensive farming methods has led to considerable interest in the health benefits of organically-produced crops and animal products. There appears to be widespread perception amongst consumers that such methods result in foods of higher nutritional quality. The present review concludes that evidence that can support or refute such perception is not available in the scientific literature. A limited number of studies have compared the nutrient compositions of organically- and conventionally-produced crops, with a very small number of studies that have compared animal products (meat, milk and dairy products) produced under the two agricultural systems. Very few compositional differences have been reported, although there are reasonably consistent findings for higher nitrate and lower vitamin C contents of conventionally-produced vegetables, particularly leafy vegetables. Data concerning possible impacts on animal and human health of diets comprising organic or conventional produce are extremely sparse. Data from controlled studies in animal models, particularly within single species, are limited or poorly designed, and findings from these studies provide conflicting conclusions. There are no reports in the literature of controlled intervention studies in human subjects. Comparison of health outcomes in populations that habitually consume organically- or conventionally-produced foods are flawed by the large number of confounding factors that might contribute to any differences reported. If consumer perceptions regarding potential health benefits of organic foods are to be supported, more research of better quality is needed than that which is currently available.

In contrast to the situation in the USA, where a wide range of genetically modified (GM) foods is available, in Europe very few GM products have been approved for marketing as foods, and there is widespread public concern about their safety and environmental impact. The marketing of a GM crop for food use in Europe falls under the EC novel foods regulations, and applications require the submission of an extensive dossier of information. The safety evaluation of GM foods presents considerable problems both in the conduct and interpretation of experimental studies, because conventional toxicity tests used in the evaluation of simple chemicals may not be appropriate for whole foods. To rationalise the safety evaluation process and to circumvent the difficulties in toxicological assessment of food materials, the concept of substantial equivalence has been developed. The concept is that if it can be demonstrated that the novel food is essentially similar to its conventional counterpart in terms of critical nutritional or anutritional components, then it is likely to be no more or less toxic than the latter. The possible introduction of unintended effects by the genetic modification process is particularly problematic for the safety evaluation process. The new genomic and post-genomic techniques are potentially valuable in the safety evaluation of GM foods, although they are as yet in their infancy.

The rapid globalization of the world economy has increased the need for a knowledge base of reliable socio-cultural differences in perceptions, values and ways of thinking about new food technologies. Awareness of socio-cultural differences is important because collaborative efforts to deal with food hazards presuppose some understanding of where, how and why the viewpoints of various stakeholders may differ. In the present paper factors that influence public perceptions of genetically-modified (GM) food are discussed, with a special focus on the unique circumstances of populations in the USA, Europe and developing countries. It is argued that effective communication and decision making about the risk of GM food depends critically on understanding how socio-cultural groups differ in their values and in the way they deal with the risks and benefits of new technologies. The implications of psychological aspects of perceived risk (including the roles of qualitative dimensions of risk, world views and trust) for public acceptance of new food technologies are highlighted.

The skills and knowledge required to carry out food allergen avoidance are becoming increasingly sophisticated. It is not enough to know the names of a handful of dishes which contain a known allergen as an ingredient. Many lifestyles now depend on food prepared away from the home. New product development has introduced a wide range of ingredients and dishes which are labour saving, exciting and innovative. Product traceability now depends on advanced technological support as it struggles to keep up with foods manufactured, prepared and served in ever more complex circumstances. Consumers are now faced with ‘a jungle of choices’. However, those individuals who need to avoid a known allergen, particularly in trace quantities, often find that the food choice deemed suitable is poor, and the information available inadequate or even dangerously misleading. There are two important groups for whom this situation is a major concern. Thousands of families with young children are forced to live with the possibility that everyday foods may be contaminated by a known allergen which could kill in minutes. They live on their nerves, reading every packet and resorting to hyperprotective childcare and vigilance. In addition, the youngest independent consumers, teenagers and those in their twenties, may have little first-hand experience of food preparation. They may be ill-equipped in food-allergen risk assessment. Sadly, those who die from anaphylaxis or allergen-triggered asthma are often in this age-group. Current initiatives to support consumers at risk include a recognised standard for manufacturers seeking to eliminate an allergen from their production, and the integration of food allergy into training for caterers and food standards enforcement professionals.

Experimental evidence indicates that the primary maternal environmental factor that regulates feto–placental growth is substrate delivery to the placental site, which is the product of maternal substrate levels and the rate of placental-bed blood flow. Thus, maternal factors which change either substrate level or flow alter feto–placental growth rate. The best-studied substrate in human pregnancy is glucose, and there is a direct relationship between maternal blood glucose levels and size at birth. Altering the type of carbohydrate eaten (high- v. low-glycaemic sources) changes postprandial glucose and insulin responses in both pregnant and non-pregnant women, and a consistent change in the type of carbohydrate eaten during pregnancy influences both the rate of feto–placental growth and maternal weight gain. Eating primarily high-glycaemic carbohydrate results in feto–placental overgrowth and excessive maternal weight gain, while intake of low-glycaemic carbohydrate produces infants with birth weights between the 25th and the 50th percentile and normal maternal weight gain. The calculated difference in energy retention with similar total energy intakes is of the order of 80 000 kJ. Preliminary information from subsequent metabolic studies indicates that the mechanisms involved include changes in: daily digestible energy requirements (i.e. metabolic efficiency), substrate utilization (glucose oxidation v. lipid oxidation), and insulin resistance and sensitivity. Thus, altering the source of maternal dietary carbohydrate may prove to be a valuable tool in the management of pregnancies at risk for anomalous feto–placental growth and for the prevention and/or treatment of obesity and insulin resistance in the non-pregnant state.

Nutrient insults in early pregnancy, such as nutrient deprivation during famines, are often associated with an unfavourable outcome. Suboptimal nutrition in the early stage of gestation has been linked to a number of adverse effects on fetal growth and development. Historically, nausea and vomiting in pregnancy (NVP) was an important contributor to pregnancy-related mortality; indeed, Charlotte Bronte died from starvation and dehydration after suffering very severe NVP 4 months into her first pregnancy (Gaskell, 1858). Although NVP seldom now progresses to be life-threatening, it affects the majority of pregnant women, and potentially presents a challenge to nutrient intake in the most vulnerable period of development. Symptoms range from mild (nausea only) to severe (a level of vomiting that restricts nutrient intake and ultimately threatens metabolic and electrolyte balance). Although NVP has been documented for thousands of years, its cause has not yet been satisfactorily elucidated, but seems to be related to endocrinological changes. Pregnant women also frequently report dietary cravings and aversions during pregnancy which can be linked to both the incidence and severity of NVP. Paradoxically, NVP appears to be positively associated with a favourable outcome of pregnancy, including increased birth weight and gestational age. The mechanisms by which NVP favours the outcome of pregnancy are not known. They may be related to women increasing their nutrient intake to alleviate symptoms, improving the quality of their diet or reducing energy expenditure. Alternatively, adaptation to a reduced nutrient intake might stimulate the expression of growth factors and affect placentation or metabolism, thus favouring fetal growth when NVP resolves.

Brain development is a complex interactive process in which early disruptive events can have long-lasting effects on later functional adaptation. It is a process that is dependent on the timely orchestration of external and internal inputs through sophisticated intra- and intercellular signalling pathways. Long-chain polyunsaturated fatty acids (LCPUFA), specifically arachidonic acid and docosahexaenoic acid (DHA), accrue rapidly in the grey matter of the brain during development, and brain fatty acid (FA) composition reflects dietary availability. Membrane lipid components can influence signal transduction cascades in various ways, which in the case of LCPUFA include the important regulatory functions mediated by the eicosanoids, and extend to long-term regulation through effects on gene transcription. Our work indicates that FA imbalance as well as specific FA deficiencies can affect development adversely, including the ability to respond to environmental stimulation. For example, although the impaired water-maze performance of mice fed a saturated-fat diet improved in response to early environmental enrichment, the brains of these animals showed less complex patterns of dendritic branching. Dietary n-3 FA deficiency influences specific neurotransmitter systems, particularly the dopamine systems of the frontal cortex. We showed that dietary deficiency of n-3 FA impaired the performance of rats on delayed matching-to-place in the water maze, a task of the type associated with prefrontal dopamine function. We did not, however, find an association over a wider range of brain DHA levels and performance on this task. Some, but not all, studies of human infants suggest that dietary DHA may play a role in cognitive development as well as in some neurodevelopmental disorders; this possibility has important implications for population health.

Epidemiological studies of human populations show that poor growth in utero predisposes an individual to the later development of type 2 (non-insulin-dependent) diabetes mellitus and hypertension in adulthood. This phenomenon is not confined to man; feeding pregnant rats diets moderately deficient in protein has a similar effect, programming the adult blood pressure and glucose metabolism of the offspring. A restriction in the amino acid supply was thought to cause poor fetal growth. However, recent experiments have shown that this is not the case and instead have implicated the metabolism of the S-containing amino acids. Many semi-synthetic experimental diets contain an imbalance in S-containing amino acids, forcing the animal to synthesise a sizeable part of its cysteine requirement from methionine. Unfortunately, when the diet is low in protein, the oxidation of amino acids is reduced, perturbing methionine metabolism and increasing levels of homocysteine. It is this interaction between protein content and composition of the diet which influences neonatal viability and may also determine the long-term health of the offspring. An excess of homocysteine is known to affect levels of two of the main mediators of cellular methylation reactions, S-adenosyl methionine and methylene tetrahydrofolate. S-adenosyl methionine is the methyl donor for the methylation of newly-synthesised DNA, regulating chromatin assembly and gene expression. The balance between S-adenosyl methionine and the methylated derivatives of folic acid may be critical for the development of differentiating cells and the long-term regulation of gene expression.

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.

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.

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.

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.

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.

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.

Developments in food technology and nutrition today are shaping our food supply in an unprecedented way. They have not only helped produce a variety of foods with varying taste and texture but also optimally retain the nutritional quality of food. Increased use of novel ingredients in the future manufacture of foods is likely to reduce the amount of micronutrients available in our diet. To combat this, food fortification may be more widely used. Collaboration between food technologists and nutritionists is imperative if we are to see the continued manufacture of wholesome food.