Increasing rates of type 2 diabetes (T2DM) follow the obesity ‘epidemic’, with 86% of patients with T2DM being overweight and over half being obese. Literature has highlighted that being overweight or obese increases the risk of diabetes. Weight loss for obese patients is associated with clinical improvements, although this evidence is mostly from short-term studies. As part of a Health Technology Assessment systematic review the long-term (≥2 years) effects of weight loss on change in diabetes-related outcome measures for those with diabetes, or risk of developing diabetes for those without diabetes, was investigated in obese individuals. Eleven studies published between 1966 and 2001 fulfilled the inclusion criteria (Caucasian, BMI >28 kg/m2, adults, no eating disorders, weight loss and changes in diabetes-outcome measures). Results of these studies indicated that intentional weight loss reduces the risk of developing diabetes in the long term and those participants with T2DM often have reduced clinical symptoms and mortality risk. These results have been verified and enhanced by literature published since this review. A similar systematic review was conducted as part of a six-phase project, the PRevent Obesity GRowing Economic Synthesis Study. This review excluded BMI >34 kg/m2 and was restricted to lifestyle interventions (or intentional weight loss). Limited information relating to diabetes was gained, with only a non-significant increasing trend for mortality from diabetes for severe weight cycling practices being suggested. Other results indicated a relationship between weight loss and fasting plasma glucose, but because of the heterogeneity of participation groups and lack of definition in relation to diabetes this relationship was not formalised. In summary, weight loss is beneficial for long-term diabetes outcomes for overweight, obese and morbidly-obese participants. There is little research evidence for those individuals who are overweight or just obese, indicating areas of future research in terms of prevention of both obesity and diabetes.

Adequate intake of folic acid by women during very early pregnancy can markedly reduce risk of the development of neural-tube defects (NTD). The effectiveness of advice to women to take folic acid supplements is limited, mainly because 50% of pregnancies are unplanned. However, mandatory folic acid food fortification programmes in North America have been very successful in reducing NTD rates. In Ireland higher rates of pregnancies are affected by NTD and the option of termination is illegal. Consequently, the much higher burden of disease makes primary prevention of NTD an important public health issue in Ireland. During 2006 a decision was taken in Ireland to initiate mandatory folic acid fortification of most bread to prevent NTD. Priority work was immediately undertaken to establish reliable and comprehensive baseline information on factors that will be affected by fortification. This information included data on: the national prevalence of pregnancies affected by NTD; the current extent of voluntary folic acid fortification of food on the Irish market and how it affects folic acid intakes; blood folate status indicators assessed for various subgroups of the Irish population. In addition, scientific developments that have arisen since 2006 relating to the risks and benefits of folic acid intake are under ongoing review. The present paper summarises the rationale for mandatory folic acid food fortification in Ireland and recent scientific developments relating to risks and benefits of folic acid intake. In this context, preliminary findings of baseline monitoring investigations in Ireland are considered.

Complex chemical processes termed non-enzymic glycation that operate in vivo and similar chemical interactions between sugars and proteins that occur during thermal processing of food (known as the Maillard reaction) are one of the interesting examples of a potentially-harmful interaction between nutrition and disease. Non-enzymic glycation comprises a series of reactions between sugars, α-oxoaldehydes and other sugar derivatives and amino groups of amino acids, peptides and proteins leading to the formation of heterogeneous moieties collectively termed advanced glycation end products (AGE). AGE possess a wide range of chemical and biological properties and play a role in diabetes-related pathology as well as in several other diseases. Diabetes is, nevertheless, of particular interest for several reasons: (1) chronic hyperglycaemia provides the substrates for extracellular glycation as well as intracellular glycation; (2) hyperglycaemia-induced oxidative stress accelerates AGE formation in the process of glycoxidation; (3) AGE-modified proteins are subject to rapid intracellular proteolytic degradation releasing free AGE adducts into the circulation where they can bind to several pro-inflammatory receptors, especially receptor of AGE; (4) kidneys, which are principally involved in the excretion of free AGE adducts, might be damaged by diabetic nephropathy, which further enhances AGE toxicity because of diminished AGE clearance. Increased dietary intake of AGE in highly-processed foods may represent an additional exogenous metabolic burden in addition to AGE already present endogenously in subjects with diabetes. Finally, inter-individual genetic and functional variability in genes encoding enzymes and receptors involved in either the formation or the degradation of AGE could have important pathogenic, nutrigenomic and nutrigenetic consequences.

Among the measures recommended by the WHO to reduce the risk of obesity and non-communicable disease, the consumption of a diet rich in micronutrients but with a relatively-low energy density features prominently. However, only a small percentage of the UK population (<1) appears to be consuming the recommended diet. Dietary behaviour is strongly influenced by the dietary environment, shaped by food supplies, investment policies and advertising, to create an obesogenic food market. Substantial resources have been invested in food production of a sort that does not promote better health; agriculture and food supply sectors have benefited from decades of public-sector support, but this practice has encouraged the production of meat, dairy, oils and sugar and the withdrawal from sale of fruit, vegetables and fish. The result is an ‘obesogenic economy’, i.e. a market economy that encourages weight gain, in which children are a prime target. Interventions in the obesogenic market need to be considered and several opportunities are described in the present paper. Recent moves to strengthen national and international food policies aimed to promote healthier behaviour have been undertaken, but they will need political support if they are to be fully implemented. Alliances of public health interests can help to create that political support and promote health-enhancing environments.

Osteoporosis is a major public health problem, and as life expectancy and the world's population continue to increase will become even more important. Thus, there is an urgent need to develop and implement nutritional approaches and policies for the prevention and treatment of osteoporosis. Patients with some chronic inflammatory diseases appear to be more likely to develop osteopenia, and in some cases earlier in life, which is of particular concern as the incidence of inflammatory diseases in the Western world is increasing. While the cause of bone loss in patients with inflammatory disease is multifactorial, nutrition may have a role. Many of these patients may have one or more nutritional deficiencies, which can lead to altered rates of bone metabolism. On the other hand, some nutritional factors may attenuate the inflammatory process itself, and thus may indirectly benefit bone metabolism and bone health in patients with inflammatory disease. The present review will consider these issues, particularly in the context of inflammatory bowel disease, coeliac diease and atherosclerosis.

Epigenetics encompasses changes to marks on the genome that are copied from one cell generation to the next, which may alter gene expression but which do not involve changes in the primary DNA sequence. These marks include DNA methylation (methylation of cytosines within CpG dinucleotides) and post-translational modifications (acetylation, methylation, phosphorylation and ubiquitination) of the histone tails protruding from nucleosome cores. The sum of genome-wide epigenetic patterns is known as the epigenome. It is hypothesised that altered epigenetic marking is a means through which evidence of environmental exposures (including nutritional status and dietary exposure) is received and recorded by the genome. At least some of these epigenetic marks are remembered through multiple cell generations and their effects may be revealed in altered gene expression and cell function. Altered epigenetic marking allows plasticity of phenotype in a fixed genotype. Despite their identical genotypes, monozygotic twins show increasing epigenetic diversity with age and with divergent lifestyles. Differences in epigenetic markings may explain some inter-individual variation in disease risk and in response to nutritional interventions.

In order to promote healthful nutrition, insight is needed into the determinants of nutrition behaviours. Behavioural determinant research and behavioural nutrition interventions have focused mostly on individual-level motivational factors. It has been argued that the individual's socio-cultural and physical environments may be the main determinants of nutrition behaviours. However, the theoretical basis and empirical evidence for environmental determinants of nutrition behaviours are not strong. The present paper is a narrative review informed by a series of systematic reviews and recent original studies on associations between environmental factors and nutrition behaviours to provide an overview and discussion of the evidence for environmental correlates and predictors of nutrition behaviour. Although the number of studies on potential environmental determinants of nutrition behaviours has increased steeply over the last decades, they include only a few well-designed studies with validated measures and guided by sound theoretical frameworks. The preliminary evidence from the available systematic reviews indicates that socio-cultural environmental factors defining what is socially acceptable, desirable and appropriate to eat may be more important for healthful eating than physical environments that define the availability and accessibility of foods. It is concluded that there is a lack of well-designed studies on environmental determinants of healthful eating behaviours. Preliminary evidence indicates that social environmental factors may be more important than physical environmental factors for healthful eating. Better-designed studies are needed to further build evidence-based theory on environmental determinants to guide the development of interventions to promote healthful eating.

The Human Genome Project and rapid advances in high-throughput molecular technologies are providing an unprecedented opportunity to advance the understanding of the common polygenic diet-related diseases, including obesity, the metabolic syndrome, type 2 diabetes mellitus, CVD and some cancers. In particular, transcriptomic approaches that allow multiple simultaneous gene-expression profiles facilitate the characterisation of metabolic perturbations that underlie diet-related pathologies. The present paper will focus on ‘transcriptomic signatures’ to characterise and understand the molecular mechanisms that accurately reflect ‘metabolic health’.

CVD is a common killer in both the Western world and the developing world. It is a multifactorial disease that is influenced by many environmental and genetic factors. Although public health advice to date has been principally in the form of prescribed population-based recommendations, this approach has been surprisingly unsuccessful in reducing CVD risk. This outcome may be explained, in part, by the extreme variability in response to dietary manipulations between individuals and interactions between diet and an individual's genetic background, which are defined by the term ‘nutrigenetics’. The shift towards personalised nutritional advice is a very attractive proposition. In principle an individual could be genotyped and given dietary advice specifically tailored to their genetic make-up. Evidence-based research into interactions between fixed genetic variants, nutrient intake and biomarkers of CVD risk is increasing, but still limited. The present paper will review the evidence for interactions between dietary fat and three common polymorphisms in the apoE, apoAI and PPARγ genes. Increased knowledge of how these and other genes influence dietary response should increase the understanding of personalised nutrition. While targeted dietary advice may have considerable potential for reducing CVD risk, the ethical issues associated with its routine use need careful consideration.