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.

The metabolic syndrome (MetS) is a key indicator of two main causes of death worldwide: CVD and diabetes. The present paper aimed to perform a review of the population-based research on the association of dietary patterns and the MetS in terms of methodology and findings. For the purpose of the present study, a scoping literature review was conducted using MEDLINE and EMBASE databases and hand searching in Google Scholar. Thirty-nine population-based studies were selected. Most of these studies used the factor analysis method and the a priori dietary approach, which had been initially extracted via a posteriori methods such as using the Mediterranean dietary pattern. The main finding was that following the Mediterranean or similar ‘healthy’ pattern reduced risk of the MetS, while following a ‘Western’ pattern increased risk of the MetS. The methodological approach in determining the dietary pattern of a population, whether a priori or a posteriori, should be chosen based on the purpose of the research. Overall, evidence suggests a diet based on the components of the Mediterranean diet and the avoidance of the ‘Western’ diet can aid in preventing the MetS.

Three areas in the brain continuously generate new neurons throughout life: the subventricular zone lining the lateral ventricles, the dentate gyrus in the hippocampus and the median eminence in the hypothalamus. These areas harbour neural stem cells, which contribute to neural repair by generating daughter cells that then become functional neurons or glia. Impaired neurogenesis leads to detrimental consequences, such as depression, decline of cognitive abilities and obesity. Adult neurogenesis is a versatile process that can be modulated either positively or negatively by many effectors, external or endogenous. Diet can modify neurogenesis both ways, either directly by ways of food-borne molecules, or possibly by the modifications induced on gut microbiota composition. It is therefore critical to define dietary strategies optimal for the maintenance of the stem cell pools.

The theory, in brief outline here, implicating deficiency of Cu in the aetiology and pathophysiology of IHD explains more attributes of the disease than any other theory. This theory satisfies several of Hill’s criteria of a half-century ago for deducing association between an environmental feature and presence of an illness. Most important is the temporal association between the rise of IHD and the decrease in dietary Cu since the 1930s along with a parallel increase in the supplementation of pregnant women with Fe, a Cu antagonist. There are more than eighty anatomical, chemical and physiological similarities between animals deficient in Cu and individuals with IHD. Few of these similarities have been produced by other dietary manipulations because feeding cholesterol induces Cu deficiency in animals. The most recent of these to be identified is decreased serum dehydroepiandrosterone. Some concomitant aspects of Cu metabolism and utilisation have been identified in other theories about heart disease: fetal programming, homocysteine, and Fe overload.

As obesity and metabolic diseases rise, there is need to investigate physiological and behavioural aspects associated with their development. Circadian rhythms have a profound influence on metabolic processes, as they prepare the body to optimise energy use and storage. Moreover, food-related signals confer temporal order to organs involved in metabolic regulation. Therefore food intake should be synchronised with the suprachiasmatic nucleus (SCN) to elaborate efficient responses to environmental challenges. Human studies suggest that a loss of synchrony between mealtime and the SCN promotes obesity and metabolic disturbances. Animal research using different paradigms has been performed to characterise the effects of timing of food intake on metabolic profiles. Therefore the purpose of the present review is to critically examine the evidence of animal studies, to provide a state of the art on metabolic findings and to assess whether the paradigms used in rodent models give the evidence to support a ‘best time’ for food intake. First we analyse and compare the current findings of studies where mealtime has been shifted out of phase from the light–dark cycle. Then, we analyse studies restricting meal times to different moments within the active period. So far animal studies correlate well with human studies, demonstrating that restricting food intake to the active phase limits metabolic disturbances produced by high-energy diets and that eating during the inactive/sleep phase leads to a worse metabolic outcome. Based on the latter we discuss the missing elements and possible mechanisms leading to the metabolic consequences, as these are still lacking.

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.

Plasma apoB is a more accurate marker of the risk of CVD and type 2 diabetes (T2D) than LDL-cholesterol; however, nutritional reviews targeting apoB are scarce. Here we reviewed eighty-seven nutritional studies and present conclusions in order of strength of evidence. Plasma apoB was reduced in all studies that induced weight loss of 6–12 % using hypoenergetic diets (seven studies; 5440–7110 kJ/d; 1300–1700 kcal/d; 34–50 % carbohydrates; 27–39 % fat; 18–24 % protein). When macronutrients were compared in isoenergetic diets (eleven studies including eight randomised controlled trials (RCT); n 1189), the diets that reduced plasma apoB were composed of 26–51 % carbohydrates, 26–46 % fat, 11–32 % protein, 10–27 % MUFA, 5–14 % PUFA and 7–13 % SFA. Replacement of carbohydrate by MUFA, not SFA, decreased plasma apoB. Moreover, dietary enriching with n-3 fatty acids (FA) (from fish: 1·1–1·7 g/d or supplementation: 3·2–3·4 g/d EPA/DHA or 4 g/d EPA), psyllium (about 8–20 g/d), phytosterols (about 2–4 g/d) or nuts (30–75 g/d) also decreased plasma apoB, mostly in hyperlipidaemic subjects. While high intake of trans-FA (4·3–9·1 %) increased plasma apoB, it is unlikely that these amounts represent usual consumption. Inconsistent data existed on the effect of soya proteins (25–30 g/d), while the positive association of alcohol consumption with low plasma apoB was reported in cross-sectional studies only. Five isoenergetic studies using Mediterranean diets (including two RCT; 823 subjects) reported a decrease of plasma apoB, while weaker evidence existed for Dietary Approaches to Stop Hypertension (DASH), vegetarian, Nordic and Palaeolithic diets. We recommend using a Mediterranean dietary pattern, which also encompasses the dietary components reported to reduce plasma apoB, to target hyperapoB and reduce the risks of CVD and T2D.

Diet-induced obesity is associated with low-grade inflammation, which, in most cases, leads to the development of metabolic disorders, primarily insulin resistance and type 2 diabetes. Although prior studies have implicated the adipose tissue as being primarily responsible for obesity-associated inflammation, the latest discoveries have correlated impairments in intestinal immune homeostasis and the mucosal barrier with increased activation of the inflammatory pathways and the development of insulin resistance. Therefore, it is essential to define the mechanisms underlying the obesity-associated gut alterations to develop therapies to prevent and treat obesity and its associated diseases. Flavonoids appear to be promising candidates among the natural preventive treatments that have been identified to date. They have been shown to protect against several diseases, including CVD and various cancers. Furthermore, they have clear anti-inflammatory properties, which have primarily been evaluated in non-intestinal models. At present, a growing body of evidence suggests that flavonoids could exert a protective role against obesity-associated pathologies by modulating inflammatory-related cellular events in the intestine and/or the composition of the microbiota populations. The present paper will review the literature to date that has described the protective effects of flavonoids on intestinal inflammation, barrier integrity and gut microbiota in studies conducted using in vivo and in vitro models.

Prevalence of type 2 diabetes mellitus (T2DM) is rapidly increasingly and is a key risk for CVD development, now recognised as the leading cause of death globally. Dietary strategies to reduce CVD development include reduction of saturated fat intake. Milk and dairy products are the largest contributors to dietary saturated fats in the UK and reduced consumption is often recommended as a strategy for risk reduction. However, overall evidence from prospective cohort studies does not confirm a detrimental association between dairy product consumption and CVD risk. The present review critically evaluates the current evidence on the association between milk and dairy products and risk of CVD, T2DM and the metabolic syndrome (collectively, cardiometabolic disease). The effects of total and individual dairy foods on cardiometabolic risk factors and new information on the effects of the food matrix on reducing fat digestion are also reviewed. It is concluded that a policy to lower SFA intake by reducing dairy food consumption to reduce cardiometabolic disease risk is likely to have limited or possibly negative effects. There remain many uncertainties, including differential effects of different dairy products and those of differing fat content. Focused and suitably designed and powered studies are needed to provide clearer evidence not only of the mechanisms involved, but how they may be beneficially influenced during milk production and processing.

Technology-based dietary assessment offers solutions to many of the limitations of traditional dietary assessment methodologies including cost, participation rates and the accuracy of data collected. The 24-h dietary recall (24HDR) method is currently the most utilised method for the collection of dietary intake data at a national level. Recently there have been many developments using web-based platforms to collect food intake data using the principles of the 24HDR method. This review identifies web- and computer-based 24HDR tools that have been developed for both children and adult population groups, and examines common design features and the methods used to investigate the performance and validity of these tools. Overall, there is generally good to strong agreement between web-based 24HDR and respective reference measures for intakes of macro- and micronutrients.

DHA is a key nutritional n-3 PUFA and needs to be supplied by the human diet. DHA is found in significant amounts in the retinal and neuronal cell membranes due to its high fluidity. Indeed, DHA is selectively concentrated in the synaptic and retinal membranes. DHA is deemed to display anti-inflammatory properties and to reduce the risk of CVD. Consumption of larger amounts of DHA appears to reduce the risk of depression, bipolar disorder, schizophrenia and mood disorders. Conversely, it has been shown that loss of DHA from the nerve cell membrane leads to dysfunction of the central nervous system in the form of anxiety, irritability, susceptibility to stress, dyslexia, impaired memory and cognitive functions, and extended reaction times. DHA plays an important role in ensuring a healthy ageing, by thwarting macular degeneration, Alzheimer’s disease, and other brain disorders at the same time as enhancing memory and strengthening neuroprotection in general. A reduced level of DHA is associated with cognitive decline during ageing. Different mechanisms for this fundamental DHA role have been put forward. Namely, neuroprotectin D1, a DHA derivative, may support brain cell survival and repair through neurotrophic, anti-apoptotic, and anti-inflammatory signalling. Many of the effects of DHA on the neurological system may be related to signalling connections, thus leading to the study of the related signalolipidomics. Therefore, the present review will focus on the influence of DHA deficiency upon ageing, with specific emphasis upon neurological disorders related to cognitive function and mental health.