A growing number of studies have shown that a diet high in long chain SFA and/or obesity cause profound changes to the energy balance centres of the hypothalamus which results in the loss of central leptin and insulin sensitivity. Insensitivity to these important anorexigenic messengers of nutritional status perpetuates the development of both obesity and peripheral insulin insensitivity. A high-fat diet induces changes in the hypothalamus that include an increase in markers of oxidative stress, inflammation, endoplasmic reticulum (ER) stress, autophagy defect and changes in the rate of apoptosis and neuronal regeneration. In addition, a number of mechanisms have recently come to light that are important in the hypothalamic control of energy balance, which could play a role in perpetuating the effect of a high-fat diet on hypothalamic dysfunction. These include: reactive oxygen species as an important second messenger, lipid metabolism, autophagy and neuronal and synaptic plasticity. The importance of nutritional activation of the Toll-like receptor 4 and the inhibitor of NF-κB kinase subunit β/NK-κB and c-Jun amino-terminal kinase 1 inflammatory pathways in linking a high-fat diet to obesity and insulin insensitivity via the hypothalamus is now widely recognised. All of the hypothalamic changes induced by a high-fat diet appear to be causally linked and inhibitors of inflammation, ER stress and autophagy defect can prevent or reverse the development of obesity pointing to potential drug targets in the prevention of obesity and metabolic dysfunction.

Tuberculosis (TB) is a major cause of mortality, responsible for 1·68 million deaths worldwide in 2009. The global prevalence of latent Mycobacterium tuberculosis infection is estimated to be 32%, and this carries a 5–20% lifetime risk of reactivation disease. The emergence of drug-resistant organisms necessitates the development of new agents to enhance the response to antimicrobial therapy for active TB. Vitamin D was used to treat TB in the pre-antibiotic era, and its active metabolite, 1,25-dihydoxyvitamin D, has long been known to enhance the immune response to mycobacteria in vitro. Vitamin D deficiency is common in patients with active TB, and several clinical trials have evaluated the role of adjunctive vitamin D supplementation in its treatment. Results of these studies are conflicting, reflecting variation between studies in baseline vitamin D status of participants, dosing regimens and outcome measures. Vitamin D deficiency is also recognised to be highly prevalent among people with latent M. tuberculosis infection in both high- and low-burden settings, and there is a wealth of observational epidemiological evidence linking vitamin D deficiency with increased risk of reactivation disease. Randomised controlled trials of vitamin D supplementation for the prevention of active TB have yet to be performed, however. The conduct of such trials is a research priority, given the safety and low cost of vitamin D supplementation, and the potentially huge public health consequences of positive results.

Coeliac disease is a permanent inflammatory disorder of the small bowel affecting approximately 1% of the population. The only effective treatment that exists is exclusion of gluten from the diet. The present paper aims to review the literature as to whether oats are safe to eat for people with coeliac disease. Much data exist on the restrictive nature that adhering to a gluten-free diet imposes on an individual. If oats could be eaten, this would help reduce the restrictive nature of the diet. This in turn could lead to an increase in the quality of life. Oats are of high-nutritional value, providing a rich source of fibre, vitamins and minerals. The fibre source contains soluble fibre which is believed to help reduce LDL-cholesterol. A systematic review of the literature was conducted. Earlier studies conducted are difficult to compare as they used different methodologies and it is not known whether samples of oats in the studies were contaminated with gluten from other cereals. Many studies reviewed do not state the strain of oat used. Recent research has suggested that it may only be in certain strains of oats which could produce a toxic response to people with coeliac disease. In conclusion, research suggests that the risk from consuming oats may be less harmful than first thought; however, may vary according to the strain of oat. Handling that risk in clinical practice remains controversial.

Obesity has been associated with low-grade systemic inflammation and with micronutrient deficiencies. Obese individuals have been found to have lower vitamin A levels and lower vitamin A intake compared with normal-weight individuals. Vitamin A plays a major role in the immune function, including innate immunity, cell-mediated immunity and humoral antibody immunity. It has also been recognised recently that vitamin A has important regulatory functions. Vitamin A status has an important effect on the chronic inflammatory response. Vitamin A deficiency increases a T-helper type 1 (Th1) response, elevates levels of pro-inflammatory cytokines, increases the expression of leptin, resistin and uncoupling proteins (UCP) and promotes adipogenesis. The effect of vitamin A deficiency on obesity might be increasing the risk of fat deposition and also the risk of chronic inflammation associated with obesity. Supplementation with vitamin A in vitro and in animal models has been found to reduce concentrations of adipocytokines, such as leptin and resistin. In conclusion, vitamin A deficiency increases a Th1 response in the presence of obesity and thus, increases the inflammatory process involved in chronic inflammation and fat deposition. The metabolism of leptin and other adipocytokines may play a critical role in the effect of vitamin A deficiency in the inflammatory response observed in obesity.

There is strong evidence indicating that excess adiposity negatively impacts immune function and host defence in obese individuals. This is a review of research findings concerning the impact of obesity on the immune response to infection, including a discussion of possible mechanisms. Obesity is characterised by a state of low-grade, chronic inflammation in addition to disturbed levels of circulating nutrients and metabolic hormones. The impact of these metabolic abnormalities on obesity-related comorbidities has undergone intense scrutiny over the past decade. However, relatively little is known of how the immune system and host defence are influenced by the pro-inflammatory and excess energy milieu of the obese. Epidemiological data suggest obese human subjects are at greater risk for nosocomial infections, especially following surgery. Additionally, the significance of altered immunity in obese human subjects is emphasised by recent studies reporting obesity to be an independent risk factor for increased morbidity and mortality following infection with the 2009 pandemic influenza A (H1N1) virus. Rodent models offer important insight into how metabolic abnormalities associated with excess body weight can impair immunity. However, more research is necessary to understand the specific aspects of immunity that are impaired and what factors are contributing to reduced immunocompetence in the obese. Additionally, special consideration of how infection in this at-risk population is managed is required, given that this population may not respond optimally to antimicrobial drugs and vaccination. Obesity impacts millions globally, and greater understanding of its associated physiological disturbances is a key public health concern.

Vitamin D insufficiency is a global issue that has significant implications for health. The classical role of vitamin D in bone mineralisation is well known; vitamin D deficiency leads to rickets, osteomalacia or osteoporosis. The role of vitamin D in an immune system is less known. Vitamin D is not an actual vitamin but a secosteroid hormone produced in the skin from 7-dehydrocholesterol after exposure to sunlight UVB radiation. Nutrition and supplements are main sources of vitamin D in wintertime in northern countries as sunlight exposure is inadequate for the production. For activation vitamin D needs to be hydroxylated in liver to form 25-hydroxyvitamin D and in kidney to 1,25-dihydroxyvitamin D, the most active hormone in Ca absorption in the gut. For determination of vitamin D status serum 25-hydroxyvitamin D level, the major circulating form of the hormone is to be measured. Vitamin D regulates gene expression through binding with vitamin D receptors, which dimerises with retinoid X receptor. This complex binds to vitamin D-responsive elements inside the promoter regions of vitamin D-responsive genes. Vitamin D has a key role in innate immunity activation; the production of antimicrobial peptides (cathelicidin and defensins) following Toll-like receptor stimulation by pathogen lipopeptides is dependent on sufficient level of 25-hydroxyvitamin D. Clinically, there is evidence of the association of vitamin D insufficiency and respiratory tract infections. There is also some evidence of the prevention of infections by vitamin D supplementation. Randomised controlled trials are warranted to explore this preventive effect.

This review will try to address the question of whether we are diagnosing too many people with coeliac disease. The key reasons for diagnosing coeliac disease may be that it is a common condition affecting up to 1% of the adult population. Delays in diagnosis are common. The average time delay reported by Coeliac UK (National Medical Patient Charity), for patients with symptoms prior to the diagnosis being made is 13 years. For every adult case detected, it is estimated that there are eight cases not detected. Patients with coeliac disease have an associated morbidity and mortality. In addition, quality of life studies suggest that the majority of patients benefit from a gluten-free diet (GFD). Furthermore, the GFD reduces or alleviates the risk of the associated complications. All of these facts could even be used to support the argument for screening! However, conversely the tests for coeliac disease are not 100% sensitive and specific. In addition, we do not know whether patients with milder symptoms will derive less benefit from treatment and are at less risk of complications. Furthermore, evidence presented in this review suggests that actual outcomes for screening studies in an adult population have revealed poor uptake and subsequently difficulties with adherence. What little published data that are available also infers that individuals recognised through screening programmes could have been detected if carefully questioned for symptoms. There is evidence to suggest that diagnosing celiac disease is cost-effective and that the diagnostic costs are offset by reduced medical expenditures, reduced hospital and general practice attendances, but this view depends on the population prevalence of coeliac disease. We believe on the basis of the evidence presented in this review that we are not diagnosing too many adults with coeliac disease. However, the authors consider case-finding with a low threshold for serological testing to be the optimal approach. If you look for coeliac disease you will find it.

In this paper we set out to explore the prevalence of child undernutrition found in community studies in affluent societies, but a preliminary literature review revealed that, in the absence of a gold standard method of diagnosis, the prevalence largely depends on the measure, threshold and the growth reference used, as well as age. We thus go on to explore describe the common clinical ‘syndromes’ of child undernutrition: wasting, stunting and failure to thrive (weight faltering) and how we have used data from two population-based cohort studies, this paper to explore how much these different ‘syndromes’ overlap and the extent to which they reflect true undernutrition. This analysis revealed that when more than one definition is applied to the same children, a majority are below the lower threshold for only one measure. However, those with both weight faltering and low BMI in infancy, go on in later childhood to show growth and body composition patterns suggestive of previous undernutrition. In older children there is even less overlap and most children with either wasting or low fat seem to be simply growing at one extreme of the normal range. We conclude that in affluent societies the diagnosis of undernutrition is only robust when it relies on a combination of both, that is decline in weight or BMI centile and wasting.

CVD still represent the greatest cause of death and disease burden in Europe and there remains uncertainty whether or not diets rich in milk and/or dairy products affect CVD risk. This paper reviews current evidence on this from prospective studies and the role of serum lipids and blood pressure as markers of CVD risk with such diets. Also the potential of animal nutrition-based approaches aimed at reducing CVD risk from consumption of milk and dairy products is outlined. Briefly, the evidence from prospective studies indicates that increased consumption of milk does not result in increased CVD risk and may give some long-term benefits, although few studies relate specifically to cheese and butter and more information on the relationship between milk/dairy product consumption and dementia is needed. Recent data suggest that the SFA in dairy products may be less of a risk factor than previously thought; although this is based on serum cholesterol responses which taken in isolation may be misleading. Milk and some dairy products have counterbalancing effects by reducing blood pressure and possibly BMI control. Despite this, animal nutrition strategies to replace some SFA in milk with cis-MUFA or cis-PUFA are extensive and intuitively beneficial, although this remains largely unproven, especially for milk. There is an urgent need for robust intervention studies to evaluate such milk-fat modifications using holistic markers of CVD risk including central arterial stiffness.