Breast cancer incidence is rising worldwide with an increase in aggressive neoplasias in young women. Possible factors involved include lifestyle changes, notably diet that is known to make an impact on gene transcription. However, among dietary factors, there is sufficient support for only greater body weight and alcohol consumption whereas numerous studies revealing an impact of specific diets and nutrients on breast cancer risk show conflicting results. Also, little information is available from middle- and low-income countries. The diversity of gene expression profiles found in breast cancers indicates that transcription control is critical for the outcome of the disease. This suggests the need for studies on nutrients that affect epigenetic mechanisms of transcription, such as DNA methylation and post-translational modifications of histones. In the present review, a new examination of the relationship between diet and breast cancer based on transcription control is proposed in light of epidemiological, animal and clinical studies. The mechanisms underlying the impact of diets on breast cancer development and factors that impede reaching clear conclusions are discussed. Understanding the interaction between nutrition and epigenetics (gene expression control via chromatin structure) is critical in light of the influence of diet during early stages of mammary gland development on breast cancer risk, suggesting a persistent effect on gene expression as shown by the influence of certain nutrients on DNA methylation. Successful development of breast cancer prevention strategies will require appropriate models, identification of biological markers for rapid assessment of preventive interventions, and coordinated worldwide research to discern the effects of diet.

Evidence from different directions, including observational and experimental studies, points to a role of vitamin D status in low-intensity chronic inflammation and insulin resistance in type 2 diabetes mellitus (T2DM). It has been recognised that insulin resistance and low-intensity chronic inflammation are risk factors for T2DM. Thus, vitamin D status can be implicated in the aetiology of TD2M. It is suggested that the relationship between vitamin D and low-intensity chronic inflammation and insulin resistance in T2DM can be mediated in part by the immune-modulating properties of the active form of vitamin D (1-α,25-dihydroxyvitamin D3; 1,25(OH)2D3), which is able to down regulate the production of pro-inflammatory cytokines – particularly TNF-α, and IL-6. However, an association between vitamin D status and these features, which is independent of BMI, has been also reported. Non-calcaemic effects of vitamin D can be associated with health outcomes other than those traditionally attributed to the vitamin.

The most frequently described drugs in the treatment of mood disorders are selective serotonin reuptake and monoamine oxidase (MAO) inhibitors, enhancing serotonin levels in the brain. However, side-effects have been reported for these drugs. Because serotonin levels in the brain are dependent on the availability of the food-derived precursor tryptophan, foods such as chicken, soyabeans, cereals, tuna, nuts and bananas may serve as an alternative to improve mood and cognition. Here we discuss the effects of high- or low-tryptophan-containing food, as well as plant extracts with a modest monoamine reuptake and MAO-A inhibition functional profile, on mood and cognition in healthy and vulnerable human subjects and rodents. Together the studies suggest that there is an inverted U-shaped curve for plasma tryptophan levels, with low and too high tryptophan levels impairing cognition, and moderate to high tryptophan levels improving cognition. This relationship is found for both healthy and vulnerable subjects. Whereas this relationship may also exist for mood, the inverted U-shaped curve for plasma tryptophan levels and mood may be based on different tryptophan concentrations in healthy v. vulnerable individuals. Animal studies are emerging and allow further understanding of effects and the mode of action of food-derived serotonergic components on mood, cognition and mechanisms. Ultimately, insight into the concentrations of tryptophan and other serotonergic components in food having beneficial effects on mood and cognition in healthy, but particularly vulnerable, subjects may support well-being in our highly demanding society.

The aim of this review was to re-assess whether the changes in energy balance that accompany pregnancy predispose parous women to obesity. A number of cross-sectional studies have sought to answer this question by examining the relationship between parity and maternal body weight. However, these studies were unable to control for the large number of sociobehavioural confounders that might be responsible for the apparent effect of parity on body weight. Longitudinal studies that examine changes in maternal body weight before and after regnancy avoid these problems by using each mother as her own control. Nevertheless, these studies have to overcome three methodological constraints: They must obtain an accurate measure of prepregnant body weight, they must give each mother sufficient time to lose any weight retained following delivery, and they must take into account the effect of ageing on maternal weight gain during pregnancy and the follow-up period. More than 90% of the studies reviewed found body weight to be greater after pregnancy than it was before (by 0.2–10.6kg). and previous researchers who have examined the evidence for pregnancy-related weight gains suggest that body weight increases by an average of 04–4.8kg following pregnancy. However, only three of the 71 longitudinal studies examined in the present review complied with the three methodological criteria. These studies concluded that mothers gain, on average, 0.9–3.3kg more weight following pregnancy than nonpregnant controls, and that mean body weight remained 0.4–3.0kg higher, even after controlling for a number of sociobehavioural confounders. This apparently modest increase in mean maternal body weight for women having one or two children conceals the fact that some mothers experience a substantial increase in body weight and become obese following pregnancy. It remains unclear whether these increases are simply the result of changes in energy metabolism during pregnancy and lactation, or whether they are influenced by inherent changes in lifestyle that accompany pregnancy and motherhood. Understanding the relative importance of these alternatives might help to explain the aetiology of maternal obesity.

“Clover was a stout motherly mare approaching middle life, who had never quite got her figure back after her fourth foal”

George Well (1945) Animal Farm. London: Secker and Warburg.

Nutrition plays an important role in osteoporosis prevention and treatment. Substantial progress in both laboratory analyses and clinical use of biochemical markers has modified the strategy of anti-osteoporotic drug development. The present review examines the use of biochemical markers in clinical research aimed at characterising the influence of foods or nutrients on bone metabolism. The two types of markers are: (i) specific hormonal factors related to bone; and (ii) bone turnover markers (BTM) that reflect bone cell metabolism. Of the former, vitamin D metabolites, parathyroid hormone, and insulin-like growth factor-I indicate responses to variations in the supply of bone-related nutrients, such as vitamin D, Ca, inorganic phosphate and protein. Thus modification in bone remodelling, the key process upon which both pharmaceutical agents and nutrients exert their anti-catabolic or anabolic actions, is revealed. Circulating BTM reflect either osteoclastic resorption or osteoblastic formation. Intervention with pharmacological agents showed that early changes in BTM predicted bone loss and subsequent osteoporotic fracture risk. New trials have documented the influence of nutrition on bone-tropic hormonal factors and BTM in adults, including situations of body-weight change, such as anorexia nervosa, and weight loss by obese subjects. In osteoporosis-prevention studies involving dietary manipulation, randomised cross-over trials are best suited to evaluate influences on bone metabolism, and insight into effects on bone metabolism may be gained within a relatively short time when biochemical markers are monitored.

The present review focuses on the specific effects of nutrients on the development of the immune system in early life. There is a big gap regarding the specific mechanisms that regulate immunity at the intestinal level and their impact in the systemic immune function. For this reason, during the last few years there has been great interest in ascertaining the mechanisms that regulate the intestinal immune function, as well as to understand how specific nutrients interact with the gut-associated lymphoid tissue. We have reviewed this topic with special emphasis on how human milk, and its components, influence the early development of intestinal immunity in breast-fed infants compared with formula-fed infants. Interactions between nutrients and intestinal microbiota have also been reviewed. Some micronutrients such as nucleotides and gangliosides, which are present in human milk and also in most foods, are able to influence immune functionality at very low concentrations. The specific action of these micronutrients on some parameters of immunity, as well as their potential mechanisms of action, have been considered in detail. However, there are limited data on how other specific nutrients, namely protein and non-protein N-containing compounds, lipids, carbohydrates, and others, such as minerals, vitamins, fibre, non-nutritional dietary compounds (flavonoids, carotenoids, phyto-oestrogens, etc), influence immunity. In the present review we have provided data regarding the potential effects of these compounds on the immune response in early life. The increasing use of functional foods by the public to improve their general health and prevent the incidence of chronic diseases has become a major area of interest within the nutrition community. Of the many functional foods available, probiotics have been most studied in infancy and childhood, particularly with regard to the prevention of allergic diseases. Infant formulae and fermented milks containing large quantities of probiotics are produced and consumed by Europeans and in other industrialized countries. In the present review we cover the clinical effects of probiotics in preventing disease during early life, as well as the potential mechanisms of interaction between probiotics and the gastrointestinal tract.

The aim of the paper is to show the various neurological and psychiatric symptoms in coeliac disease (CD). CD is a T cell-mediated, tissue-specific autoimmune disease which affects genetically susceptible individuals after dietary exposure to proline- and glutamine-rich proteins contained in certain cereal grains. Genetics, environmental factors and different immune systems, together with the presence of auto-antigens, are taken into account when identifying the pathogenesis of CD. CD pathogenesis is related to immune dysregulation, which involves the gastrointestinal system, and the extra-intestinal systems such as the nervous system, whose neurological symptoms are evidenced in CD patients. A gluten-free diet (GFD) could avoid cerebellar ataxia, epilepsy, neuropathies, migraine and mild cognitive impairment. Furthermore, untreated CD patients have more symptoms and psychiatric co-morbidities than those treated with a GFD. Common psychiatric symptoms in untreated CD adult patients include depression, apathy, anxiety, and irritability and schizophrenia is also common in untreated CD. Several studies show improvement in psychiatric symptoms after the start of a GFD. The present review discusses the state of the art regarding neurological and psychiatric complications in CD and highlights the evidence supporting a role for GFD in reducing neurological and psychiatric complications.

The anatomical structure and function of beaks, bills and tongue together with the mechanics of deglutition in birds have contributed to the development of a taste system denuded of macrostructures visible to the human naked eye. Studies in chickens and other birds have revealed that the avian taste system consists of taste buds not clustered in papillae and located mainly (60 %) in the upper palate hidden in the crevasses of the salivary ducts. That explains the long delay in the understanding of the avian taste system. However, recent studies reported 767 taste buds in the oral cavity of the chicken. Chickens appear to have an acute sense of taste allowing for the discrimination of dietary amino acids, fatty acids, sugars, quinine, Ca and salt among others. However, chickens and other birds have small repertoires of bitter taste receptors (T2R) and are missing the T1R2 (related to sweet taste in mammals). Thus, T1R2-independent mechanisms of glucose sensing might be particularly relevant in chickens. The chicken umami receptor (T1R1/T1R3) responds to amino acids such as alanine and serine (known to stimulate the umami receptor in rodents and fish). Recently, the avian nutrient chemosensory system has been found in the gastrointestinal tract and hypothalamus related to the enteroendocrine system which mediates the gut–brain dialogue relevant to the control of feed intake. Overall, the understanding of the avian taste system provides novel and robust tools to improve avian nutrition.

Obesity is a risk factor for asthma, and obese asthmatics have lower disease control and increased symptom severity. Several putative links have been proposed, including genetics, mechanical restriction of the chest and the intake of corticosteroids. The most consistent evidence, however, comes from studies of cytokines produced by the adipose tissue called adipokines. Adipokine imbalance is associated with both proinflammatory status and asthma. Although reverse causation has been proposed, it is now acknowledged that obesity precedes asthma symptoms. Nevertheless, prenatal origins of both conditions complicate the search for causality. There is a confirmed role of neuro-immune cross-talk mediating obesity-induced asthma, with leptin playing a key role in these processes. Obesity-induced asthma is now considered a distinct asthma phenotype. In fact, it is one of the most important determinants of asthma phenotypes. Two main subphenotypes have been distinguished. The first phenotype, which affects adult women, is characterised by later onset and is more likely to be non-atopic. The childhood obesity-induced asthma phenotype is characterised by primary and predominantly atopic asthma. In obesity-induced asthma, the immune responses are shifted towards T helper (Th) 1 polarisation rather than the typical atopic Th2 immunological profile. Moreover, obese asthmatics might respond differently to environmental triggers. The high cost of treatment of obesity-related asthma, and the burden it causes for the patients and their families call for urgent intervention. Phenotype-specific approaches seem to be crucial for the success of prevention and treatment.

Some amino acids (AA) act through several signalling pathways and mechanisms to mediate the control of gene expression at the translation level, and the regulation occurs, specifically, on the initiation and the signalling pathways for translation. The translation of mRNA to protein synthesis proceeds through the steps of initiation and elongation, and AA act as important feed-forward activators that are involved in many pathways, such as the sensing and the transportation of AA by cells, in these steps in many tissues of mammals. For the translation, phosphorylation of eukaryotic translation initiation factor 2α (eIF2α) is a critical molecule that controls the translation initiation and its functions can be regulated by some AA. Another control point in the mRNA binding step in the translation initiation is at the regulation by mammalian target of rapamycin, which requires a change of phosphorylation status of ribosomal protein S6. In fact, the change of phosphorylation status of ribosomal protein S6 might be involved in global protein synthesis. The present review summarises recent work on the molecular mechanisms of the regulation of protein synthesis by AA and highlights new findings.

The most widely used pharmacological therapies for obesity and weight management are based on inhibition of gastrointestinal lipases, resulting in a reduced energy yield of ingested foods by reducing dietary lipid absorption. Colipase-dependent pancreatic lipase is believed to be the major gastrointestinal enzyme involved in catalysis of lipid ester bonds. There is scant literature on the action of pancreatic lipase under the range of physiological conditions that occur within the human small intestine, and the literature that does exist is often contradictory. Due to the importance of pancreatic lipase activity to nutrition and weight management, the present review aims to assess the current body of knowledge with regards to the physiology behind the action of this unique gastrointestinal enzyme system. Existing data would suggest that pancreatic lipase activity is affected by intestinal pH, the presence of colipase and bile salts, but not by the physiological range of Ca ion concentration (as is commonly assumed). The control of secretion of pancreatic lipase and its associated factors appears to be driven by gastrointestinal luminal content, particularly the presence of acid or digested proteins and fats in the duodenal lumen. Secretion of colipase, bile acids and pancreatic lipase is driven by cholecystokinin and secretin release.

Homelessness is present in most societies and represents a situation in which the basic needs for survival including food are often limited. It is logical to surmise that the homeless person’s diet is likely to be nutritionally deficient and yet there is a relative paucity in research regarding this issue with studies varying in both their methodology and homeless population. Despite these differences, diets of the homeless are frequently characterised as high in saturated fat and deficient in fibre and certain micronutrients, all of which can have negative implications for the homeless individual’s health and/or mental state. The conclusion from intervention studies is that there is no consensus as to the most effective method for assessing dietary intake. In order to address this, the present review aims to provide a greater understanding of the existing literature surrounding nutrition and the homeless and to act as a foundation from which further research can be conducted. An evaluation of the main findings and challenges surrounding the assessment of the nutritional status of the homeless will be provided followed by a review of the physical and mental consequences of the homeless diet. Current and potential interventions aimed at increasing the nutritional quality of food consumed by the homeless will be addressed with a focus on the role of the nutritional science community in assisting in this endeavour.