More than a century ago, two Nobel Prizes in Physiology and Medicine were awarded to scientists who established the link between microbes and human health.

Cocoa, a product consumed since 600 BC, is now a subject of increasing interest because of its antioxidant properties, which are mainly attributed to the content of flavonoids such as ( − )-epicatechin, catechin and procyanidins. Moreover, recent findings suggest a regulatory effect of cocoa on the immune cells implicated in innate and acquired immunity. Cocoa exerts regulatory activity on the secretion of inflammatory mediators from macrophages and other leucocytes in vitro. In addition, emerging data from in vivo studies support an immunomodulating effect. Long-term cocoa intake in rats affects both intestinal and systemic immune function. Studies in this line suggest that high-dose cocoa intake in young rats favours the T helper 1 (Th1) response and increases intestinal γδ T lymphocyte count, whereas the antibody-secreting response decreases. The mechanisms involved in this activity are uncertain; nonetheless, because redox-sensitive pathways control immune cell function, the action of cocoa flavonoids on modulating cell signalling and gene expression deserves investigation.

Inflammation is a stereotypical physiological response to infections and tissue injury; it initiates pathogen killing as well as tissue repair processes and helps to restore homeostasis at infected or damaged sites. Acute inflammatory reactions are usually self-limiting and resolve rapidly, due to the involvement of negative feedback mechanisms. Thus, regulated inflammatory responses are essential to remain healthy and maintain homeostasis. However, inflammatory responses that fail to regulate themselves can become chronic and contribute to the perpetuation and progression of disease. Characteristics typical of chronic inflammatory responses underlying the pathophysiology of several disorders include loss of barrier function, responsiveness to a normally benign stimulus, infiltration of inflammatory cells into compartments where they are not normally found in such high numbers, and overproduction of oxidants, cytokines, chemokines, eicosanoids and matrix metalloproteinases. The levels of these mediators amplify the inflammatory response, are destructive and contribute to the clinical symptoms. Various dietary components including long chain ω-3 fatty acids, antioxidant vitamins, plant flavonoids, prebiotics and probiotics have the potential to modulate predisposition to chronic inflammatory conditions and may have a role in their therapy. These components act through a variety of mechanisms including decreasing inflammatory mediator production through effects on cell signaling and gene expression (ω-3 fatty acids, vitamin E, plant flavonoids), reducing the production of damaging oxidants (vitamin E and other antioxidants), and promoting gut barrier function and anti-inflammatory responses (prebiotics and probiotics). However, in general really strong evidence of benefit to human health through anti-inflammatory actions is lacking for most of these dietary components. Thus, further studies addressing efficacy in humans linked to studies providing greater understanding of the mechanisms of action involved are required.

Workers in the Nutrition Society offices in London have recently uncovered an announcement from 1946 highlighting the launch of the British Journal of Nutrition.

There is substantial evidence which shows that constraints in the early life environment are an important determinant of risk of metabolic disease and CVD. There is emerging evidence that higher birth weight, which reflects a more abundant prenatal environment, is associated with increased risk of cancer, in particular breast cancer and childhood leukaemia. Using specific examples from epidemiology and experimental studies, this review discusses the hypothesis that increased susceptibility to CVD, metabolic disease and cancer have a common origin in developmental changes induced in the developing fetus by aspects of the intra-uterine environment including nutrition which involve stable changes to the epigenetic regulation of specific genes. However, the induction of specific disease risk is dependent upon the nature of the environmental challenge and interactions between the susceptibility set by the altered epigenome and the environment throughout the life course.

Over recent months I have been approached by authors of accepted or already published papers with requests to remove an author or to add an author.

Human milk is a complex physiological fluid that provides nutrients as well as bioactive factors for the infant(1). A distinctive property of human milk among all other species is its remarkable content and structural diversity of oligosaccharides(2–4).

The aim of the present observational study was to investigate the relationships between glycaemic status and levels of oxidative stress and inflammation in well-controlled type 2 diabetes subjects. Metabolic variables (weight, BMI, waist circumference (waist), blood glucose, glycated Hb (HbA1c), insulin, blood lipids), biomarkers of oxidative stress (8-iso-PGF2α, malondialdehyde, 8-oxo-7,8-dihydro-2′-deoxyguanosine, formamido pyrimidine glycosylase-sites, frequency of micronucleated erythrocytes, nitrotyrosine) and inflammatory markers (high sensitivity C-reactive protein (hsCRP), IL-6, cyclo-oxygenase-catalyzed PGF2α-metabolite) were measured. Fifty-six patients (thirty women and twenty-six men, age 62·3 (sd 7·0) years, HbA1c 6·1 (sd 0·9) %, BMI 28·3 (sd 3·8) kg/m2, waist 99·6 (sd 11·1) cm) were included in the study. HbA1c (r 0·29, P = 0·03) and blood glucose (r 0·33, P = 0·01) correlated positively with 8-iso-PGF2α. Positive correlations were also observed between HbA1c and nitrotyrosine (r 0·42, P = 0·01), waist and hsCRP (r 0·37, P = 0·005), hsCRP and IL-6 (r 0·61, P < 0·0001) and between PGF2α-metabolite and 8-iso-PGF2α (r 0·27, P = 0·048). The present study indicates that glycaemic status is associated with oxidative stress even in subjects with well-controlled type 2 diabetes. Furthermore, inflammation was more related to abdominal obesity than to glycaemic control. A large number of biomarkers of oxidative stress and inflammation were investigated, but only a few associations were found between the markers. This could be due to the fact that none of these biomarkers biosynthesises via similar pathways or simultaneously owing to their diverse nature and origin.

Central nervous system leptin resistance as a possible cause of obesity and associated diseases is a ‘hot topic’ in nutrition research. Simultaneously, a new field in biomedical sciences has evolved during the past years.

CVD is a major cause of mortality and morbidity in the Western world. In recent years its importance has expanded internationally and it is believed that by 2020 it will be the biggest cause of mortality in the world, emphasising the importance to prevent or minimise this increase. A beneficial role for vitamins in CVD has long been explored but the data are still inconsistent. While being supported by observational studies, randomised controlled trials have not yet supported a role for vitamins in primary or secondary prevention of CVD and have in some cases even indicated increased mortality in those with pre-existing late-stage atherosclerosis. The superiority of combination therapy over single supplementation has been suggested but this has not been confirmed in trials. Studies have indicated that β-carotene mediates pro-oxidant effects and it has been suggested that its negative effects may diminish the beneficial effects mediated by the other vitamins in the supplementation cocktail. The trials that used a combination of vitamins that include β-carotene have been disappointing. However, vitamin E and vitamin C have in combination shown long-term anti-atherogenic effects but their combined effect on clinical endpoints has been inconsistent. Studies also suggest that vitamins would be beneficial to individuals who are antioxidant-deficient or exposed to increased levels of oxidative stress, for example, smokers, diabetics and elderly patients, emphasising the importance of subgroup targeting. Through defining the right population group and the optimal vitamin combination we could potentially find a future role for vitamins in CVD.

An inverse association between alcohol consumption and risk of CHD in diverse populations has been reported in over forty prospective studies(1).

A role of dietary nutrients in relation to insulin resistance has been suggested but conclusive evidence in human beings is lacking. Asian Indians and South Asians are prone to develop insulin resistance and the metabolic syndrome. In the present paper, data pertaining to nutrient intake, insulin resistance and cardiovascular risk factors in Asian Indians and South Asians have been reviewed. In these populations, several dietary imbalances have been reported: low intake of MUFA, n-3 PUFA and fibre, and high intake of fats, saturated fats, carbohydrates and trans-fatty acids (mostly related to the widespread use of Vanaspati, a hydrogenated oil). Some data suggest that these nutrient imbalances are associated with insulin resistance, dyslipidaemia and subclinical inflammation in South Asians. Specifically, in children and young individuals, a high intake of n-6 PUFA is correlated with fasting hyperinsulinaemia, and in adults, high-carbohydrate meal consumption was reported to cause hyperinsulinaemia, postprandial hyperglycaemia and hypertriacylglycerolaemia. Dietary supplementation with n-3 PUFA leads to an improved lipid profile but not insulin sensitivity. Inadequate maternal nutrition in pregnancy, low birth weight and childhood ‘catch-up’ obesity may be important for the development of the metabolic syndrome and diabetes. Even in rural populations, who usually consume traditional frugal diets, there is an increasing prevalence of cardiovascular risk factors and the metabolic syndrome due to changes in diets and lifestyle. Nationwide community intervention programmes aimed at creating awareness about the consequences of unhealthy food choices and replacing them by healthy food choices are urgently needed in urban and rural populations in India, other countries in South Asia and in migrant South Asians.

Hypertension or high blood pressure is a significant health problem worldwide. Typically, lifestyle changes, including adopting a healthy diet, are recommended for people with an elevated blood pressure. Lactotripeptides are bioactive milk peptides with potential antihypertensive properties in man. These peptides, as part of a food product or as nutraceutical, may contribute to the prevention and treatment of hypertension. This paper reviews the current evidence of the blood pressure control properties of lactotripeptides in man. Blood pressure-lowering effects of lactotripeptides are typically measured after 4–6 weeks of treatment. However, in some cases, a blood pressure response has been observed after 1–2 weeks. Maximum blood pressure reductions approximate 13 mmHg (systolic blood pressure) and 8 mmHg (diastolic blood pressure) after active treatment compared with placebo, and are likely reached after 8–12 weeks of treatment. Effective dosages of lactotripeptides range from 3·07 to 52·5 mg/d. Evidence indicates that lactotripeptides are only effective at elevated blood pressure; no further lowering of normal blood pressure has been observed. Concomitant intake of antihypertensive medication does not seem to influence the potency of lactotripeptides to lower blood pressure. Similarly, ethnicity has not been found to influence the extent of lactotripeptide-induced blood pressure lowering. Based on the currently available data, lactotripeptides appear to be safe and effective. Thus, they can be part of a healthy diet and lifestyle to prevent or reduce high blood pressure.

Folic acid plays an essential role in DNA and methionine metabolism. Micro-organisms in the rumen can synthesise folates, but it has not been verified that these amounts are sufficient to achieve the best efficiency of dairy cows. However, the amount of folates synthesised in the rumen could possibly, to some extent, be affected by the forage:concentrate ratio. Degradation of orally supplemented folic acid in the rumen seems to be very high (about 97 %), as supplementation of folic acid hardly increases folate concentrations in the digesta at the duodenum. However, it must be considered that dietary supplements of folic acid higher than 0·5 mg/kg body weight increased serum folate concentrations in all available studies and milk folate concentrations in most studies. Additionally, milk production tended to be increased in some studies. Therefore, degradation of folic acid in the rumen may be overestimated as folates can be absorbed at the proximal duodenum. For future research it is necessary to consider the whole flow and the metabolic pathways of folates from the rumen to duodenum, blood, tissue, milk and transfer to calf to declare requirement values for cows. Consequently, the present review discusses current knowledge and emphasises areas for future research.

Links between nutrition and cognition are widely acknowledged. Within the context of short-term cognitive performance, carbohydrate has been the dietary component most commonly investigated. The majority of studies investigating the influence of carbohydrate on cognitive performance have employed oral glucose drink interventions followed by measures of performance on cognitive tests. More recently, studies have investigated the effect of different carbohydrates on cognitive performance rather than just pure glucose drinks. To date, studies have not been evaluated based on a standardised measure of glycaemic response, such as glycaemic load. The present review provides a critical evaluation of eight studies that have explored the relationships between food carbohydrate and cognitive performance and allow glycaemic load to be used as a basis for comparison. The key finding is that these provide insufficient evidence to support a consistent effect of glycaemic load on short-term cognitive performance. Future studies should employ consistent test methodologies and describe food interventions in more detail to facilitate meaningful comparisons and interpretations of results.

Long-chain n-3 PUFA are considered important for cardiovascular health and brain development. Meat other than fish contributes significantly to total intakes of long-chain n-3 PUFA in adults; however, there are limited published data examining the intake of individual meat sources in children and adolescents in the Australian population. A review of literature was conducted using PubMed, Agricola and CAB Abstracts using the terms ‘intake’, ‘beef’, ‘lamb’, ‘pork’, ‘poultry’, ‘fish’, ‘children’ and ‘adolescents’ and using reference lists in published articles. Studies and surveys were identified that contained published values for intakes of meat or fish. Two national dietary surveys of children and adolescents were conducted in Australia in 1985 and 1995 and two regional surveys were conducted in Western Sydney and Western Australia in 1994 and 2003, respectively. Comprehensive data for the intake of individual meat sources were not reported from the 1995 survey, but estimations of intake were calculated from published values. Reported intakes of meat and fish are generally lower in females than males and tend to increase with age. Weighted mean intakes of red meat (beef plus lamb) across the three most recent studies were 67·3 and 52·2 g/d, respectively, for males and females aged between 7 and 12 years and 87·7 and 54·2 g/d, respectively, for males and females aged 12–18 years. These weighted intakes are within Australian guidelines and are likely to contribute significantly to total long-chain n-3 PUFA intake in children and adolescents in the Australian population.

Nutrition is important to bone health, and a number of minerals and vitamins have been identified as playing a potential role in the prevention of bone diseases, particularly osteoporosis. Despite this, there is currently no consensus on maximum levels to allow in food or as dietary supplements. The benefits of supplementation of populations at risk of osteoporosis with Ca and vitamin D are well established. Prolonged supplementation of Ca and vitamin D in elderly has been shown to prevent bone loss, and in some intervention studies to prevent fragility fractures. Although P is essential to bone health, the average intake is considered to be more than sufficient and supplementation could raise intake to adverse levels. The role of vitamin K in bone health is less well defined, though it may enhance the actions of Ca and vitamin D. Sr administered in pharmacological doses as the ranelate salt was shown to prevent fragility fractures in postmenopausal osteoporosis. However, there is no hard evidence that supplementation with Sr salts would be beneficial in the general population. Mg is a nutrient implicated in bone quality, but the benefit of supplementation via foodstuffs remains to be established. A consensus on dietary supplementation for bone health should balance the risks, for example, exposure of vulnerable populations to values close to maximal tolerated doses, against evidence for benefits from randomised clinical trials, such as those for Ca and vitamin D. Feedback from community studies should direct further investigations and help formulate a consensus on dietary supplementation for bone health.