Adolescent pregnancy is a major public health challenge for many industrialised countries and is associated with significant medical, nutritional, social and economic risk for mothers and their infants. Despite this, relatively little is known about the nutrient intakes of adolescents during pregnancy. The aim of this study is to review the current evidence relating to the dietary assessment of pregnant adolescents living in industrialised countries. Nine papers were identified that fulfilled the inclusion criteria, seven of which were conducted in the USA. Mean nutrient intakes were compared with the most recent US dietary reference intakes (DRI) for pregnant adolescents. Despite the poor quality of the majority of studies, there appeared to be some consensus to suggest that the nutrient intakes of pregnant adolescents were below the DRI for energy, iron, folate, calcium, vitamin E and magnesium, nutrients which are recognised to be vital for fetal growth and development during pregnancy. Modest differences were observed in nutrient intake between trimesters and age groups. Current research is limited by sampling and measurement bias, and research is urgently required to address these limitations. Further consideration should also be made of the influence of age and of role of socio-economic support on pregnant adolescents' nutrient intake. The achievement of improved nutrition in pregnancy among adolescents requires multidisciplinary collaborations of adolescent health care providers, academics, professional organisations, policy makers, industry and service users. Only once this is achieved can adolescent nutrition, and adolescent nutrition in pregnancy, be significantly and sustainably optimised.

The coordinated regulation of metabolic fuel selection is crucial to energy homeostasis. Philip Randle and his colleagues developed the fundamental concept of interplay between carbohydrate and lipid fuels in relation to the requirement for energy utilisation and storage. Their insight has fashioned current understanding of the regulation of metabolism in health and disease, as well as providing a springboard for research into the roles of lipid derivatives in insulin resistance and, at the transcriptional level, lipid-regulated nuclear hormone receptors.

Nutritional genomics is a new and promising science area which can broadly be defined as the application of high throughput genomics (transcriptomics, proteomics, metabolomics/metabonomics) and functional genomic technologies to the study of nutritional sciences and food technology. First utilised in the food industry by plant biotechnologists to manipulate plant biosynthetic pathways, the use of genomic technologies has now spread within the agriculture sector, unleashing a host of new applications (e.g. approaches for producing novel, non-transgenic plant varietals; identification of genetic markers to guide plant and animal breeding programmes; exploration of diet–gene interactions for enhancing product quality and plant/animal health). Beyond agriculture, genomic technologies are also contributing to the improvement of food processing, food safety and quality assurance as well as the development of functional food products and the evolution of new health management concepts such as ‘personalised nutrition’, an emerging paradigm in which the diet of an individual is customised, based on their own genomic information, to optimise health and prevent disease. In this review the relevance of nutritional genomics to the food industry will be considered and examples given on how this science area is starting to be leveraged for economic benefits and to improve human nutrition and health.

The literature on predefined indexes of overall diet quality is reviewed. Their association with nutrient adequacy and health outcome is considered, but our primary interest is in the make-up of the scores. In total, twenty different indexes have been reviewed, four of which have gained most attention, and many others were based on those four. The various scores differ in many respects, such as the items included, the cut-off values used, and the exact method of scoring, indicating that many arbitrary choices have been made. Correlations in intake between dietary components may not be adequately addressed. In general, diet quality scores show an association with mortality or disease risk, but these relations are generally modest. Existing indexes do not predict morbidity or mortality significantly better than individual dietary factors. Although conclusions from the review may provide guidance in the construction of a diet quality score, it is questionable whether a dietary score can be obtained that is a much better predictor of health outcome.

Pancreatic polypeptide (PP) is a gut hormone released from the pancreas in response to food ingestion and remains elevated for up to 6 h postprandially. Plasma levels are elevated in patients with pancreatic tumours. An intravenous infusion of PP has been reported to reduce food intake in man, suggesting that PP is a satiety hormone. We investigated whether a lower infusion rate of PP would induce significant alterations in energy intake. The study was randomised and double-blinded. Fourteen lean fasted volunteers (five men and nine women) received 90 min infusions of PP (5 pmol/kg per min) and saline on two separate days. The dose chosen was half that used in a previous human study which reported a decrease in appetite but at supra-physiological levels of PP. One hour after the end of the infusion, a buffet lunch was served and energy intake measured. PP infusion was associated with a significant 11 % reduction in energy intake compared with saline (2440 (se 200) v. 2730 (se 180) kJ; P < 0·05). Preprandial hunger as assessed by a visual analogue score was decreased in the PP-treated group compared to saline. These effects were achieved with plasma levels of PP within the pathophysiological range of pancreatic tumours.

There is considerable evidence for the induction of different phenotypes by variations in the early life environment, including nutrition, which in man is associated with a graded risk of metabolic disease; fetal programming. It is likely that the induction of persistent changes to tissue structure and function by differences in the early life environment involves life-long alterations to the regulation of gene transcription. This view is supported by both studies of human subjects and animal models. The mechanism which underlies such changes to gene expression is now beginning to be understood. In the present review we discuss the role of changes in the epigenetic regulation of transcription, specifically DNA methylation and covalent modification of histones, in the induction of an altered phenotype by nutritional constraint in early life. The demonstration of altered epigenetic regulation of genes in phenotype induction suggests the possibility of interventions to modify long-term disease risk associated with unbalanced nutrition in early life.

Growth failure is a common yet complex problem of childhood chronic kidney disease caused by multiple factors encountered due to the primary disease or secondary to the renal impairment. This review seeks to describe the various patho-physiological mechanisms contributing to growth failure in the various stages of childhood with particular emphasis on nutritional problems and endocrine dysfunction encountered whilst managing these children. In addition, we shall examine the role of body composition in chronic kidney disease, their relationship with growth and nutrition and the potential effect of abnormalities in fat mass and lean mass on long-term morbidity and mortality.

High alcohol consumption is related to colorectal cancer (CRC). Our objective was to study associations between alcohol consumption and risk of CRC according to characteristics of aetiological pathways: the chromosomal instability (CIN) and the microsatellite instability (MIN) pathway. We classified CIN+ tumours (tumours with either a truncating APC mutation, an activating K-ras mutation or overexpression of p53), MIN+ tumours (tumours lacking hMLH1 expression) and CIN− /MIN−  tumours (tumours without these defects). In the Netherlands Cohort Study on diet and cancer, 120 852 men and women, aged 55–69 years, completed a questionnaire on risk factors for cancer at baseline (1986). Case–cohort analyses were conducted using 573 CRC cases with complete data after 7·3 years of follow-up, excluding the first 2·3 years. Adjusted incidence rate ratios (RR) and 95 % confidence intervals (CI) were estimated. Compared with abstaining, alcohol consumption of ≥ 30 g/d was positively associated with the risk of CRC irrespective of genetic or molecular aberrations present, although statistical significance was not reached (RR 1·35 (95 % CI 0·9–2·0) for the CIN+ tumours, RR 1·59 (95 % CI 0·4–5·8) for the MIN+ tumours and RR 1.15 (95 % CI 0·5–2·7) for the CIN− /MIN−  tumours). Beer, wine and liquor consumption were, independent of their alcoholic content, not consistently associated with the risk of CRC within the defined subgroups. In conclusion, our results indicate that a daily alcohol consumption of ≥ 30 g is associated with an increase in risk of CRC, independent of the presence or absence of the studied characteristics of different aetiological pathways.

In 1995, Anderson et al. published a meta-analysis, derived from most of the clinical studies on soya proteins given to individuals with varying levels of cholesterolaemia that had been reported up to that time. The meta-analysis clearly indicated that cholesterolaemias were generally reduced by diets with soya given as a partial or total substitution of animal proteins, with final mean total and LDL-cholesterol reductions of 23·2 mg/dl and 21·7 mg/dl, respectively. These findings were recently strongly criticised, based on the evaluation of later studies, frequently involving individuals with normal or moderately elevated cholesterolaemias. In the present paper, these more recent studies were re-evaluated using a ‘nomogram’ prepared on the basis of the quartiles of initial cholesterol concentrations in the Anderson meta-analysis and their corresponding CI for net cholesterol change. The five studies belonging to the first quartile and thirteen out of the fourteen belonging to the second quartile gave results perfectly in line with the nomogram. Out of the fourteen studies belonging to the third quartile, ten agreed with the nomogram and two gave lower cholesterol reductions, whereas two gave higher reductions. Unfortunately, none of the recent studies belonged to the fourth quartile as treatment with statins or other lipid-lowering drugs is now mandatory in the presence of very high cholesterol levels. The re-evaluation thus shows that the thirty-three studies published in the past 10 years are in agreement with the Anderson meta-analysis and confirm its validity.

Tomatoes are rich in lycopene and other carotenoids which have shown beneficial effects on CVD in epidemiological and intervention studies. In the present study the effect of an extract of lycopene-rich tomatoes, Lyc-O-Mato® on atherosclerosis was studied in Watanabe Heritable Hyperlipidemic rabbits. The rabbits were fed a control diet, a control diet supplemented with the tomato extract or a control diet supplemented with a mixture of plant oils for 16 weeks. Lycopene was detected only in plasma of rabbits receiving tomato extract. The tomato extract had no effect on cholesterol and triacylglycerol levels measured in total plasma, lipoprotein fractions and on aortic atherosclerosis evaluated biochemically and by microscopy. Oxidation of lipids in unfractionated plasma also was unaffected by the intake of tomato extract. In conclusion, the tomato extract increased plasma levels of lycopene in rabbits, but had no effect on hypercholesterolaemia, oxidation of plasma lipids or aortic atherosclerosis.

Commercial milk is homogenized for the purpose of physical stability, thereby reducing fat droplet size and including caseins and some whey proteins at the droplet interface. This seems to result in a better digestibility than untreated milk. Various casein peptides and milk fat globule membrane (MFGM) proteins are reported to present either harmful (e.g. atherogenic) or beneficial bioactivity (e.g. hypotensive, anticarcinogenic and others). Homogenization might enhance either of these effects, but this remains controversial. The effect of homogenization has not been studied regarding the link between early cow's milk consumption and occurrence of type I diabetes in children prone to the disease and no link appears in the general population. Homogenization does not influence milk allergy and intolerance in allergic children and lactose-intolerant or milk-hypersensitive adults. The impact of homogenization, as well as heating and other treatments such as cheesemaking processes, on the health properties of milk and dairy products remains to be fully elucidated.

An association between Ca intake and the risk of prostate cancer has been reported in some but not all epidemiological studies. Assuming that a pathophysiological relationship would underlie this association, a favoured hypothesis proposes that relatively high Ca consumption could promote prostate cancer by reducing the production of 1,25-dihydroxyvitamin D (1,25(OH)2D; calcitriol), the hormonal form of vitamin D. The present review analyses the plausibility of this hypothesis by considering the quantitative relationships linking Ca intake to 1,25(OH)2D production and action in healthy conditions and in prostate cancer. Changes in the plasma level of 1,25(OH)2D in response to Ca intake are of very small magnitude as compared with the variations required to influence the proliferation and differentiation of prostate cancer cells. In most studies, 1,25(OH)2D plasma level was not found to be reduced in patients with prostate cancer. The possibility that the level of 1,25(OH)2D in prostate cells is decreased with a high-Ca diet has not been documented. Furthermore, a recent randomised placebo-controlled trial did not indicate that Ca supplementation increases the relative risk of prostate cancer in men. In conclusion, the existence of a pathophysiological link between relatively high Ca intake and consequent low production and circulation level of 1,25(OH)2D that might promote the development of prostate cancer in men remains so far an hypothesis, the plausibility of which is not supported by the analysis of available clinical data.

Cu and Fe metabolism are known to be linked, but the interactions during pregnancy are less well studied. In the present study we used rats to examine the effect of Cu deficiency during pregnancy on Fe and Cu levels in maternal and fetal tissue and on the gene expression profile of proteins involved in Cu and Fe metabolism in the placenta. Rats were fed diets with different Cu contents before and during pregnancy. Samples were collected on day 21 of gestation. Cu levels, ceruloplasmin activity and serum Fe all decreased in maternal serum of Cu-deficient animals. Maternal liver Fe inversely correlated with liver Cu. Placental Cu levels decreased with no change in Fe. Fe and Cu levels both decreased in the fetal liver. The drop in maternal liver Cu was significantly correlated with a decrease in organ weight of fetal liver, lung and kidney. No changes were observed in mRNA expression of Cu transporter 1, Menkes P-type Cu-ATPase 7A, Wilson P-type Cu-ATPase 7B, cytochrome-c oxidase, and Cu chaperone Atox1 in the placenta of Cu-deficient dams. Transferrin receptor 1 and the Fe-responsive element (IRE)-regulated divalent metal transporter 1 (DMT1) were up regulated; while ferroportin and non-IRE1-regulated DMT1 levels did not change. These data show that Cu deficiency during pregnancy not only has a direct effect on Fe levels but also regulates the expression of Fe transporters. The pattern closely mirrors that seen in Fe deficiency, suggesting that the changes are a consequence of the decrease in serum Fe, implying that the developing fetus not only suffers from Cu, but also from Fe deficiency.