The assay features of biochemical markers of bone turnover have markedly improved in the past few years. The most sensitive and specific markers of bone formation include serum bone alkaline phosphatase, total osteocalcin (including the intact molecule and the large N-mid fragment) and the procollagen type I N-terminal propeptide assay. Among the various markers of bone resorption, measurements of the urinary excretion of N- and C-terminal cross-linked telopeptides) and of serum C-terminal cross-linked telopeptides are the most sensitive and specific. Markers of bone turnover can be used to predict the rate of bone loss in post-menopausal women and can also be used to assess the risk of fractures. In osteoporosis-treatment studies (with alendronate, risedronate, raloxifene) markers of bone turnover appear even more strongly associated with fracture risk reduction than bone mineral density (BMD). These observations support the use of markers of bone turnover as surrogates for fracture risk reduction, perhaps even more so than BMD. Bone markers can also be used to monitor the efficacy of antiresorptive therapy such as hormone-replacement therapy, raloxifene and bisphosphonates in individual patients. Furthermore, they have also proved to be helpful in monitoring the response to nutritional interventions and have the advantage over BMD in that they provide information about mechanism of effect and changes are often observed much more rapidly.

Obesity in children is difficult to treat, but it seems to be easier to treat than adult obesity. The first step in treatment is to identify effective advice relating to nutrition and physical activity. In most treatment studies the macronutrient composition of the diet is not of major importance for treatment outcome. In relation to physical activity fat-utilisation strategies have been described. The second step includes appropriate approaches to lifestyle change. In Europe there are no drugs approved for children, and surgery for children is still limited to research projects. Thus, the major challenge is to develop effective ways of changing lifestyle. Family therapy may be an effective approach in preventing severe obesity from developing during puberty, and a therapeutic strategy based on treatment studies is described. The family-therapy techniques used here are intended to facilitate the family's own attempts to modify their lifestyle, and to increase their own sense of responsibility and readiness to change, i.e. these variables are the prime targets during therapy. Thus, the family, not the therapist, assumes responsibility for the changes achieved. This approach may be helpful in making the therapeutic process less cumbersome for the therapist. Instead of the therapist attempting to persuade the obese subjects to lose weight, it might be more effective to teach them to control their eating patterns through their own efforts. The treatment model includes structural family therapy and solution-focused-brief therapy. The use of such a model makes it possible to train therapists and health professionals to use an evidence-based intervention model.

Previous studies have shown that consumption of fruit and vegetables plays a role in preventing the onset of CVD. These beneficial effects have been linked to the presence of polyphenolic compounds in plant-derived foods and their antioxidant capacity. It has been hypothesised that polyphenols may also have a direct effect on vascular endothelial cell growth and the expression of genes involved in angiogenesis and other roles of the endothelium. Previous studies in this area have tended to use concentrations of polyphenols that are supraphysiological (1–100 μm). The effects of more physiological concentrations (0·1 μm) of various individual polyphenols on gene expression were therefore investigated in cultured human umbilical vein endothelial cells (HUVEC) using both microarray and quantitative RT–PCR methodologies. Treatment of HUVEC with ferulic acid, quercetin or resveratrol (0·1 μm) resulted in changes to gene expression that for the three treatments amounted to significant (>2-fold) down-regulation of the expression of 363 genes and significant (>2-fold) up-regulation of 233 genes of the 10 000 genes present on the microarray. The majority of these genes were affected by resveratrol. Quantitative RT–PCR studies indicated that resveratrol (0·1 μm) significantly increased the expression of the gene encoding endothelial NO synthase (eNOS), which synthesises the vasodilator molecule NO, and both resveratrol and quercetin decreased expression of the potent vasoconstrictor, endothelin-1 (ET-1), while ferulic acid had no effect. The effects of resveratrol (0·1 μm) were also investigated when HUVEC were under oxidative stress following treatment with H2O2 (0–50 μm), which dose-dependently increased expression of eNOS and ET-1. Resveratrol stimulated eNOS mRNA in the absence of H2O2 and still allowed the increase with H2O2, but the effects were not additive. In contrast, resveratrol blocked the stimulatory effect of H2O2 on ET-1 expression. Hence, resveratrol has potent effects at a physiological concentration (0·1 μm) that would be expected to result in vasodilation and therefore help reduce blood pressure and the risk of CVD.

There is now considerable evidence from several data sources, including the National Surveys of Lifestyles, Attitudes and Nutrition, that dietary patterns vary according to social position in the Republic of Ireland and those individuals in situations of social disadvantage experience barriers to consuming a healthy diet according to recommended guidelines. Obesity is a major impending public health problem related in part to social position that requires concerted inter-sectoral policy action. The Life-ways Cross-generation Cohort Study of >1000 Irish families has been followed prospectively since antenatal recruitment in 2001. Published findings to date indicate considerable social variability in food consumption and BMI patterns during pregnancy in the case of the maternal cohort. The present paper reports nutrient intake across the four family cohorts related to a key variable of interest, means-tested General Medical Services eligibility.

The beneficial effects of long-chain (C chain ≥20) n-3 PUFA are well documented and, overall, increased intake reduces risk of CVD. Recent evidence also points to a role in reducing age-related decline in cognitive function. The two key fatty acids are EPA (20:5) and DHA (22:6), with current UK recommendation for adults being 450 mg EPA+DHA/d. Whilst some EPA and DHA can be synthesised in vivo from α-linolenic acid, recent data indicate this source to be very limited, suggesting that EPA and DHA should be classified as dietary essentials. In many parts of Europe the daily intake of EPA+DHA by adults and especially young adults (18–24 years) is <100 mg/d, since many never eat oily fish. Poultry meat contributes small but worthwhile amounts of EPA+DHA. Studies to enrich the EPA+DHA content of animal-derived foods mainly use fish oil in the diet of the animal. Recent work has shown that such enrichment has the potential to provide to the UK adult diet a daily intake of EPA+DHA of about 230 mg, with poultry meat providing the largest amount (74 mg). There are, however, concerns that the continued and possibly increased use of fish oils in animals' diets is not sustainable and alternative approaches are being examined, including the genetic modification of certain plants to allow them to synthesise EPA and DHA from shorter-chain precursors.

Throughout the life cycle the skeleton requires optimum development and maintenance of its integrity to prevent fracture. Bones break because the loads placed on them exceed the ability of the bone to absorb the energy involved. It is now estimated that one in three women and one in twelve men aged >55 years will suffer from osteoporosis in their lifetime and at a cost in the UK of >£1·7×109 per year. The pathogenesis of osteoporosis is multifactorial. Both the development of peak bone mass and the rate of bone loss are determined by key endogenous and exogenous factors. Ca supplements appear to be effective in reducing bone loss in women late post menopause (>5 years post menopause), particularly in those with low habitual Ca intake (<400 mg/d). In women early post menopause (<5 years post menopause) who are not vitamin D deficient, Ca supplementation has little effect on bone mineral density. However, supplementation with vitamin D and Ca has been shown to reduce fracture rates in the institutionalised elderly, but there remains controversy as to whether supplementation is effective in reducing fracture in free-living populations. Re-defining vitamin D requirements in the UK is needed since there is evidence of extensive hypovitaminosis D in the UK. Low vitamin D status is associated with an increased risk of falling and a variety of other health outcomes and is an area that requires urgent attention. The role of other micronutrients on bone remains to be fully defined, although there are promising data in the literature for a clear link between vitamin K nutrition and skeletal integrity, including fracture reduction.