Undernutrition profoundly affects immune responses, particularly at the extremities of life: in infants and in the elderly. The present review focuses on this interrelationship in the elderly. It describes three different stages of ageing: stage 1, healthy ageing, which is observed in very healthy elderly individuals who have no nutritional deficit; stage 2, common ageing, which is observed in most elderly individuals in whom various micronutrient deficits are found; stage 3, pathological ageing, which is observed in patients with protein–energy deficiency. Stage 1, primary immune ageing, is essentially characterized by changes in T-cell subsets but no change in T-cell function; T-cell function is reduced only in the very elderly (>90 years old). Stage 2, secondary immune ageing, is influenced by micronutrient deficits that may be corrected by providing nutritional supplements. Furthermore, immune responses may also be enhanced by supplementation of subjects who have no micronutrient deficits, indicating that the immune system of elderly individuals is highly susceptible to the influence of micronutrients. In stage 3, tertiary immune ageing, the immune responses are strongly related to the decreased nutritional status. In these patients decreased immune responses lead to long-lasting acute-phase responses, which induce greater use of nutritional reserves during disease and lead to increased frailty. As nutritional status has a marked effect on immune responses in elderly individuals, nutritional therapy should be given to elderly individuals who have nutrient deficits, and perhaps also to individuals who do not have nutrient deficits in order to promote healthy ageing and extend the lifespan.

The present paper presents the approach, results and outcome of an innovative piece of action research amongst professionals (health and non-health) and the public (women and young people from low-income families in one of the deprived areas of Birmingham, UK). A cooperative inquiry approach was used and data were collected on concerns about health of professionals (n 15) and the public (n 19), as well as dietary practices, smoking pattern and access to healthy foods amongst the public (n 49). The methods of data collection were: desk research; observation; semi-structured individual and focus-group interviews; structured individual interviews. The findings highlight diverse views and expectations about health amongst the public and the professionals, and suggest the existence of tensions between the partnership and the ownership of inter-agency collaboration. It argues the importance of having a shared vision amongst health and non-health professionals regarding health strategy and the way forward for working together to promote the public's health. It recommends that by using the tenet of action research, and adapting a cooperative inquiry approach, members of a partnership project could learn through reflection on action and achieve personal development and social action.

The environment encountered in fetal and neonatal life exerts a profound influence on physiological function and risk of disease in adult life. Epidemiological evidence suggests that impaired fetal growth followed by rapid catch-up in infancy is a strong predictor of obesity, hypertension, non-insulin-dependent diabetes and CHD. Whilst these associations have been widely accepted to be the product of nutritional factors operating in pregnancy, evidence from human populations to support this assertion is scarce. Animal studies clearly demonstrate that there is a direct association between nutrient imbalance in fetal life and later disease states, including hypertension, diabetes, obesity and renal disease. These associations are independent of changes in fetal growth rates. Experimental studies examining the impact of micro- or macronutrient restriction and excess in rodent pregnancy provide clues to the mechanisms that link fetal nutrition to permanent physiological changes that promote disease. Exposure to glucocorticoids in early life appears to be an important consequence of nutrient imbalance and may lead to alterations in gene expression that have major effects on tissue development and function. Epigenetic mechanisms, including DNA methylation, may also be important processes in early-life programming.

The present paper reflects a practical activity undertaken by the Nutrition Society's qualitative research network in October 2005. It reflects the structure of that exercise. First, there is an introduction to feminist methodology and methods. The informing premise is that feminist methodology is of particular interest to practitioners (professional and/or academic) engaged in occupations numerically dominated by women, such as nutritionists. A critical argument is made for a place for feminist methodology in related areas of social research. The discussion points to the differences that exist between various feminist commentators, although the central aims of feminist research are broadly shared. The paper comprises an overview of organizing concepts, discussion and questions posed to stimulate discussion on the design and process of research informed by feminist methodology. Issues arising from that discussion are summarized.

The increase in CVD incidence following the menopause is associated with oestrogen loss. Dietary isoflavones are thought to be cardioprotective via their oestrogenic and oestrogen receptor-independent effects, but evidence to support this role is scarce. Individual variation in response to diet may be considerable and can obscure potential beneficial effects in a sample population; in particular, the response to isoflavone treatment may vary according to genotype and equol-production status. The effects of isoflavone supplementation (50 mg/d) on a range of established and novel biomarkers of CVD, including markers of lipid and glucose metabolism and inflammatory biomarkers, have been investigated in a placebo-controlled 2×8-week randomised cross-over study in 117 healthy post-menopausal women. Responsiveness to isoflavone supplementation according to (1) single nucleotide polymorphisms in a range of key CVD genes, including oestrogen receptor (ER) α and β and (2) equol-production status has been examined. Isoflavones supplementation was found to have no effect on markers of lipids and glucose metabolism. Isoflavones improve C-reactive protein concentrations but do not affect other plasma inflammatory markers. There are no differences in response to isoflavones according to equol-production status. However, differences in HDL-cholesterol and vascular cell adhesion molecule 1 response to isoflavones v. placebo are evident with specific ERβ genotypes. In conclusion, isoflavones have beneficial effects on C-reactive protein, but not other cardiovascular risk markers. However, specific ERβ gene polymorphic subgroups may benefit from isoflavone supplementation.

Studies have shown that the risk of hypertension in adulthood can be affected by the in utero environment. It is established that hypertension is linked to compromised kidney function and that factors affecting organogenesis can increase the risk of later disease. Prostaglandins (PG) and growth factors are known to play an important role in regulating kidney function and renal organogenesis. The extent, however, to which global energy restriction (where all nutrients are reduced) of the mother can programme later blood pressure control or renal PG and growth factor status is unknown. A study is described that aimed to examine the long-term effects of maternal nutrient restriction (NR) and elucidate their relationship with compromised kidney development. First, it was necessary to establish animal models. A sheep model of 50% NR during specific stages of gestation was used to investigate fetal renal development, whilst a rat model of 50% NR throughout pregnancy was used to investigate postnatal kidney development and adult functioning. Molecular analysis has shown that expression of the growth hormone–insulin-like growth factor (GH–IGF) axis is affected by NR in the fetal sheep kidneys, and that changes are dependent on the timing of NR and whether the fetus is a singleton or a twin. Analysis of the kidneys from the rat model has shown nutritional differences in the expression of PG receptors and the enzymes responsible for PG synthesis and degradation that persist into adulthood. In conclusion, NR does affect the GH–IGF and PG axes, and these changes may be important in the nutritional programming of renal functioning and adult blood pressure control.

There is growing evidence that the type of carbohydrate consumed is important in relation to metabolic disease risk, and there is currently particular interest in the role of low-glycaemic-index (GI) foods. Observational studies have associated low-GI diets with decreased risk of type 2 diabetes and CHD, and improvements in various metabolic risk factors have been seen in some intervention studies. However, findings have been mixed and inconsistent. There are a number of plausible mechanisms for the effects of these foods on disease risk, which arise from the differing metabolic responses to low- and high-GI foods, with low-GI foods resulting in reductions in hyperglycaemia, hyperinsulinaemia and late postprandial circulating NEFA levels. Low-GI foods may also increase satiety and delay the return of hunger compared with high-GI foods, which could translate into reduced energy intake at later time points. However, the impact of a low-GI diet on body weight is controversial, with many studies confounded by dietary manipulations that differ in aspects other than GI. There is currently much interest in GI from scientists, health professionals and the public, but more research is needed before clear conclusions can be drawn about relationships with metabolic disease risk.

Cruciferous vegetables have been studied extensively for their chemoprotective effects. Although they contain many bioactive compounds, the anti-carcinogenic actions of cruciferous vegetables are commonly attributed to their content of glucosinolates. Glucosinolates are relatively biologically inert but can be hydrolysed to a range of bioactive compounds such as isothiocyanates (ITC) and indoles by the plant-based enzyme myrosinase, or less efficiently by the colonic microflora. A number of mechanisms whereby ITC and indoles may protect against colo-rectal cancer have been identified. In experimental animals cruciferous vegetables have been shown to inhibit chemically-induced colon cancer. However, the results of recent epidemiological cohort studies have been inconsistent and this disparity may reflect a lack of sensitivity of such studies. Possible explanations for the failure of epidemiological studies to detect an effect include: assessment of cruciferous vegetable intake by methods that are subject to large measurement errors; the interaction between diet and genotype has not been considered: the effect that post-harvest treatments may have on biological effects of cruciferous vegetables has not been taken into account.