The brain has a high metabolic rate and its metabolism is almost entirely restricted to oxidative utilisation of glucose. These factors emphasise the extreme dependence of neural tissue on a stable and adequate supply of glucose. Whereas initially it was thought that only glucose deprivation (i.e. under hypoglycaemic conditions) can affect brain function, it has become apparent that low-level fluctuations in central availability can affect neural and consequently, cognitive performance. In the present paper the impact of diet-based glycaemic response and glucose regulation on cognitive processes across the lifespan will be reviewed. The data suggest that although an acute rise in blood glucose levels has some short-term improvements of cognitive function, a more stable blood glucose profile, which avoids greater peaks and troughs in circulating glucose is associated with better cognitive function and a lower risk of cognitive impairments in the longer term. Therefore, a habitual diet that secures optimal glucose delivery to the brain in the fed and fasting states should be most advantageous for the maintenance of cognitive function. Although the evidence to date is promising, it is insufficient to allow firm and evidence-based nutritional recommendations. The rise in obesity, diabetes and metabolic syndrome in recent years highlights the need for targeted dietary and lifestyle strategies to promote healthy lifestyle and brain function across the lifespan and for future generations. Consequently, there is an urgent need for hypothesis-driven, randomised controlled trials that evaluate the role of different glycaemic manipulations on cognition.

Valid estimation of usual dietary intake in epidemiological studies is a topic of present interest. The aim of the present paper is to review recent literature on innovative approaches focussing on: (1) the requirements to assess usual intake and (2) the application in large-scale settings. Recently, a number of technology-based self-administered tools have been developed, including short-term instruments such as web-based 24-h recalls, mobile food records or simple closed-ended questionnaires that assess the food intake of the previous 24 h. Due to their advantages in terms of feasibility and cost-effectiveness these tools may be superior to conventional assessment methods in large-scale settings. New statistical methods have been developed to combine dietary information from repeated 24-h dietary recalls and FFQ. Conceptually, these statistical methods presume that the usual food intake of a subject equals the probability of consuming a food on a given day, multiplied by the average amount of intake of that food on a typical consumption day. Repeated 24-h recalls from the same individual provide information on consumption probability and amount. In addition, the FFQ can add information on intake frequency of rarely consumed foods. It has been suggested that this combined approach may provide high-quality dietary information. A promising direction for estimation of usual intake in large-scale settings is the integration of both statistical methods and new technologies. Studies are warranted to assess the validity of estimated usual intake in comparison with biomarkers.

Current dietary assessment methods including FFQ, 24-h recalls and weighed food diaries are associated with many measurement errors. In an attempt to overcome some of these errors, dietary biomarkers have emerged as a complementary approach to these traditional methods. Metabolomics has developed as a key technology for the identification of new dietary biomarkers and to date, metabolomic-based approaches have led to the identification of a number of putative biomarkers. The three approaches generally employed when using metabolomics in dietary biomarker discovery are: (i) acute interventions where participants consume specific amounts of a test food, (ii) cohort studies where metabolic profiles are compared between consumers and non-consumers of a specific food and (iii) the analysis of dietary patterns and metabolic profiles to identify nutritypes and biomarkers. The present review critiques the current literature in terms of the approaches used for dietary biomarker discovery and gives a detailed overview of the currently proposed biomarkers, highlighting steps needed for their full validation. Furthermore, the present review also evaluates areas such as current databases and software tools, which are needed to advance the interpretation of results and therefore enhance the utility of dietary biomarkers in nutrition research.

A wide range of health benefits have been ascribed to soya intake including a lowered risk of osteoporosis, heart disease, breast cancer, and menopausal symptoms. Because it is a hormonally active diet, however, soya can also be endocrine disrupting, suggesting that intake has the potential to cause adverse health effects in certain circumstances, particularly when exposure occurs during development. Consequently, the question of whether or not soya phyto-oestrogens are beneficial or harmful to human health is neither straightforward nor universally applicable to all groups. Possible benefits and risks depend on age, health status, and even the presence or absence of specific gut microflora. As global consumption increases, greater awareness and consideration of the endocrine-disrupting properties of soya by nutrition specialists and other health practitioners is needed. Consumption by infants and small children is of particular concern because their hormone-sensitive organs, including the brain and reproductive system, are still undergoing sexual differentiation and maturation. Thus, their susceptibility to the endocrine-disrupting activities of soya phyto-oestrogens may be especially high. As oestrogen receptor partial agonists with molecular and cellular properties similar to anthropogenic endocrine disruptors such as bisphenol A, the soya phyto-oestrogens provide an interesting model for how attitudes about what is ‘synthetic’ v. what is ‘natural,’ shapes understanding and perception of what it means for a compound to be endocrine disrupting and/or potentially harmful. This review describes the endocrine-disrupting properties of soya phyto-oestrogens with a focus on neuroendocrine development and behaviour.

Complex, diverse and rarely appearing without comorbidity, the autism spectrum disorders continue to be a source of research interest. With core symptoms variably impacting on social communication skills, the traditional focus of many research efforts has centred on the brain and how genetic and environmental processes impact on brain structure, function and/or connectivity to account for various behavioural presentations. Alongside emerging ideas on autistic traits being present in various clinical states, the autisms, and the overrepresentation of several comorbid conditions impacting on quality of life, other research avenues have opened up. The central role of the brain in relation to autism may be at least partially influenced by the functions of other organs. The gastrointestinal (GI) tract represents an important biological system pertinent to at least some autism. The notion of a gut–brain–behaviour axis has garnered support from various findings: an overrepresentation of functional and pathological bowel states, bowel and behavioural findings showing bidirectional associations, a possible relationship between diet, GI function and autism and recently, greater focus on aspects of the GI tract such as the collected gut microbiota in relation to autism. Gaps remain in our knowledge of the functions of the GI tract linked to autism, specifically regarding mechanisms of action onward to behavioural presentation. Set however within the context of diversity in the presentation of autism, science appears to be moving towards defining important GI-related autism phenotypes with the possibility of promising dietary and other related intervention options onward to improving quality of life.

Nutrient profiling (NP) models rate the nutritional quality of individual foods, based on their nutrient composition. Their goal is to identify nutrient-rich foods, generally defined as those that contain more nutrients than calories and are low in fat, sugar and salt. NP models have provided the scientific basis for evaluating nutrition and health claims and regulating marketing and advertising to children. The food industry has used NP methods to reformulate product portfolios. To help define what we mean by healthy foods, NP models need to be based on published nutrition standards, mandated serving sizes and open-source nutrient composition databases. Specifically, the development and testing of NP models for public health should follow the seven decision steps outlined by the European Food Safety Authority. Consistent with this scheme, the nutrient-rich food (NRF) family of indices was based on a variable number of qualifying nutrients (from six to fifteen) and on three disqualifying nutrients (saturated fat, added sugar, sodium). The selection of nutrients and daily reference amounts followed nutrient standards for the USA. The base of calculation was 418·4 kJ (100 kcal), in preference to 100 g, or serving sizes. The NRF algorithms, based on unweighted sums of percent daily values, subtracted negative (LIM) from positive (NRn) subscores (NRn – LIM). NRF model performance was tested with respect to energy density and independent measures of a healthy diet. Whereas past uses of NP modelling have been regulatory or educational, voluntary product reformulation by the food industry may have most impact on public health.

Recent re-evaluations of dietary reference values (DRV) for vitamin D have established intake requirements between 10 and 20 µg/d. National nutrition surveys indicate that habitual mean intakes of vitamin D in the population are typically in the range 3–7 µg/d. As vitamin D supplementation will not be effective at a population level because the uptake is generally low, creative food-based solutions are needed to bridge the gap between current intakes and these new requirement values. The overarching aim of this review is to highlight how food-based solutions can have an important role in bridging this gap and counteracting vitamin D inadequacy in Europe and elsewhere. The present review initially briefly overviews very recent new European DRV for vitamin D and, while not in agreement on requirement estimates, how they point very clearly to the need for food-based solutions. The review discusses the need for traditional fortification of foods in the dairy and other sectors, and finally overviews recent advances in the area of biofortification of food with vitamin D. In conclusion, increasing vitamin D intakes across the population distribution is important from a public health perspective to reduce the high degree of inadequacy of vitamin D intake in Europe. Fortification, including biofortification, of a wider range of foods, which accommodate diversity, is likely to have the potential to increase vitamin D intakes across the population distribution. Research has had, and will continue to have, a key role in terms of developing food-based solutions and tackling vitamin D deficiency.

Epidemiological data on consumption of flavonoid-containing food points to the notion that some of these secondary plant metabolites may favour healthy ageing. The aim of the present paper was to review the literature on lifespan extension by flavonoids in worms, flies and mice. In most studies, worms and flies experienced lifespan extension when supplemented with flavonoids either as extracts or single compounds. Studies with mutant worms and flies give hints as to which gene products may be regulated by flavonoids and consequently enhance longevity. We discuss the data considering putative mechanisms that may underlie flavonoid action such as energy-restriction-like effects, inhibition of insulin-like-growth-factor signalling, induction of antioxidant defence mechanisms, hormesis as well as antimicrobial properties. However, it remains uncertain whether human lifespan could be prolonged by increased flavonoid intake.

Polyphenols are ubiquitous secondary products present in many plant foods. Their intake has been associated with health benefits ranging from reduced incidence of CVD, diabetes and cancers to improved neurodegenerative outcomes. Major dietary sources include beverages such as coffee, teas and foods such as chocolate. Fruits are also major sources and berries in particular are a palatable source of a diverse range of polyphenol components. There are a number of ways that polyphenol uptake could be increased and healthier polyphenol-rich foods could be produced with specific compositions to target-specific health effects. Firstly, we could exploit the genetic diversity of plants (with a focus on berries) to select varieties that have enhanced levels of specific polyphenols implicated in disease mitigation (e.g. anthocyanins, tannins or flavonols). Working with variation induced by environmental and agronomic factors, modern molecular breeding techniques could exploit natural variation and beneficially alter polyphenol content and composition, although this could be relatively long term. Alternatively, we could employ a synthetic biology approach and design new plants that overexpress certain genes or re-deploy more metabolic effort into specific polyphenols. However, such ‘polyphenol-plus’ fruit could prove unpalatable as polyphenols contribute to sensorial properties (e.g. astringency of tannins). However, if the aim was to produce a polyphenol as a pharmaceutical then ‘lifting’ biosynthetic pathways from plants and expressing them in microbial vectors may be a feasible option. Secondly, we could design processing methods to enhance the polyphenolic composition or content of foods. Fermentation of teas, cocoa beans and grapes, or roasting of cocoa and coffee beans has long been used and can massively influence polyphenol composition and potential bioactivity. Simple methods such as milling, heat treatment, pasteurisation or juicing (v. pureeing) can have notable effects on polyphenol profiles and novel extraction methods bring new opportunities. Encapsulation methods can protect specific polyphenols during digestion and increase their delivery in the gastrointestinal tract to target-specific health effects. Lastly we could examine reformulation of products to alter polyphenol content or composition. Enhancing staple apple or citrus juices with berry juices could double polyphenol levels and provide specific polyphenol components. Reformulation of foods with polyphenol-rich factions recovered from ‘wastes’ could increase polyphenol intake, alter product acceptability, improve shelf life and prevent food spoilage. Finally, co-formulation of foods can influence bioavailability and potential bioactivity of certain polyphenols. Within the constraints that certain polyphenols can interfere with drug effectiveness through altered metabolism, this provides another avenue to enhance polyphenol intake and potential effectiveness. In conclusion, these approaches could be developed separately or in combination to produce foods with enhanced levels of phenolic components that are effective against specific disease conditions.

In this paper, I first provide definitions of nutrient profiling and of a nutrient profile model. I set out the purposes of nutrient profiling: both general and specific. I give two examples of nutrient profile models that have been developed for regulatory purposes by the Food Standards Agency (FSA) in the UK and the WHO for its European Region – the UK FSA/Ofcom and the WHO-Euro models – and compare the way the models are constructed and function, how they have been developed, the extent to which they have been tested and validated and their use in regulation. Finally I draw some conclusions about the future use of nutrient profiling for regulatory purposes. I argue that its full potential has yet to be realised and give some reasons why. I pose some urgent research questions with respect to nutrient profiling.

Chronic pancreatitis is a chronic inflammatory disease of the pancreas characterised by irreversible morphological change and typically causing pain and/or permanent loss of function. This progressive, irreversible disease results in destruction of healthy pancreatic tissue and the development of fibrous scar tissue. Gradual loss of exocrine and endocrine function follows, along with clinical manifestations such as steatorrhoea, abdominal pain and diabetes. Nutrition in chronic pancreatitis has been described as a problem area and, until recently, there was little research on the topic. It is often asserted that >90 % of the pancreas must be damaged before exocrine insufficiency occurs; however, an exploration of the original studies from the 1970s found that the data do not support this assertion. The management of steatorrhoea with pancreatic enzyme replacement therapy is the mainstay of nutritional management, and early identification and treatment is a key. The presence of steatorrhoea, coupled with poor dietary intake (due to intractable abdominal pain, gastrointestinal side effects and often alcoholism) renders the chronic pancreatitis patients at considerable risk for undernutrition, muscle depletion and fat-soluble vitamin deficiency. Premature osteoporosis/osteopenia afflicts two-thirds of patients as a consequence of poor dietary intake of calcium and vitamin D, low physical activity, low sunlight exposure, heavy smoking, as well as chronic low-grade inflammation. Bone metabolism studies show increased bone formation as well as bone resorption in chronic pancreatitis, indicating that bone turnover is abnormally high. Loss of the pancreatic islet cells occurs later in the disease process as the endocrine cells are diffusely distributed throughout the pancreatic parenchyma. Patients may develop type 3c (pancreatogenic) diabetes, which is complicated by concurrent decreased glucagon secretion, and hence an increased risk of hypoglycaemia. Diabetes control is further complicated by poor diet, malabsorption and (for some) alcoholism, and therefore those with type 3c diabetes have clinical characteristics and therapeutic goals that are different from that of type 1 and type 2 diabetes patients. This review describes emerging research and clinical guidelines for nutrition in chronic pancreatitis.