With the substantial economic and social burden of CVD, the need to modify diet and lifestyle factors to reduce risk has become increasingly important. Milk and dairy products, being one of the main contributors to SFA intake in the UK, are a potential target for dietary SFA reduction. Supplementation of the dairy cow's diet with a source of MUFA or PUFA may have beneficial effects on consumers' CVD risk by partially replacing milk SFA, thus reducing entry of SFA into the food chain. A total of nine chronic human intervention studies have used dairy products, modified through bovine feeding, to establish their effect on CVD risk markers. Of these studies, the majority utilised modified butter as their primary test product and used changes in blood cholesterol concentrations as their main risk marker. Of the eight studies that measured blood cholesterol, four reported a significant reduction in total and LDL-cholesterol (LDL-C) following chronic consumption of modified milk and dairy products. Data from one study suggested that a significant reduction in LDL-C could be achieved in both the healthy and hypercholesterolaemic population. Thus, evidence from these studies suggests that consumption of milk and dairy products with modified fatty acid composition, compared with milk and dairy products of typical milk fat composition, may be beneficial to CVD risk in healthy and hypercholesterolaemic individuals. However, current evidence is insufficient and further work is needed to investigate the complex role of milk and cheese in CVD risk and explore the use of novel markers of CVD risk.

Cognitive decline may lead to dementia whose most frequent cause is Alzheimer's disease (AD). Among the many potential risk factors of cognitive decline and AD, diet raises increasing interest. Most studies considered diet in the frame of a single nutrient approach with inconsistent results. A novel approach to examine the link between nutrition and cognitive function is the use of dietary patterns. The aim of the present review was to update and complete the body of knowledge about dietary patterns in relationship with various cognitive outcomes in the elderly. Two approaches can be used: a priori and a posteriori patterns. A priori patterns are defined by the adhesion to a pre-defined healthy diet using a score such as the Mediterranean diet (MeDi) score, the Healthy Eating Index, the Canadian Healthy Eating Index, the French National Nutrition and Health Programme (Programme National Nutrition Santé) Guideline Score (PNNS-GS), the Recommended Food Score (RFS) and Dietary Approaches to Stop Hypertension (DASH). MeDi score, RFS, PNNS-GS and DASH have been associated with lower risks of cognitive impairment, cognitive decline, and dementia or AD. Principal components analysis, reduced rank regression and clustering methods allow the identification of ‘healthy’ patterns associated with lower risk of cognitive decline. However, some studies did not report any associations with cognitive outcomes and results are discordant especially regarding MeDi and the risk of dementia. Several methodological challenges should be overcome to provide a higher level of evidence supporting the development of nutritional policies to prevent cognitive decline and AD.

The alarming prevalence of obesity has led to a better understanding of the molecular mechanisms controlling energy homeostasis. Regulation of energy intake and expenditure is more complex than previously thought, being influenced by signals from many peripheral tissues. In this sense, a wide variety of peripheral signals derived from different organs contributes to the regulation of body weight and energy expenditure. Besides the well-known role of insulin and adipokines, such as leptin and adiponectin, in the regulation of energy homeostasis, signals from other tissues not previously thought to play a role in body weight regulation have emerged in recent years. The role of fibroblast growth factor 21 (FGF21), insulin-like growth factor 1 (IGF-I), and sex hormone-binding globulin (SHBG) produced by the liver in the regulation of body weight and insulin sensitivity has been recently described. Moreover, molecules expressed by skeletal muscle such as myostatin have also been involved in adipose tissue regulation. Better known is the involvement of ghrelin, cholecystokinin, glucagon-like peptide 1 (GLP-1) and PYY3–36, produced by the gut, in energy homeostasis. Even the kidney, through the production of renin, appears to regulate body weight, with mice lacking this hormone exhibiting resistance to diet-induced obesity. In addition, the skeleton has recently emerged as an endocrine organ, with effects on body weight control and glucose homeostasis through the actions of bone-derived factors such as osteocalcin and osteopontin. The comprehension of these signals will help in a better understanding of the aetiopathology of obesity, contributing to the potential development of new therapeutic targets aimed at tackling excess body fat accumulation.

Reducing elevated LDL-cholesterol is a key public health challenge. There is substantial evidence from randomised controlled trials (RCT) that a number of foods and food components can significantly reduce LDL-cholesterol. Data from RCT have been reviewed to determine whether effects are additive when two or more of these components are consumed together. Typically components, such as plant stanols and sterols, soya protein, β-glucans and tree nuts, when consumed individually at their target rate, reduce LDL-cholesterol by 3–9 %. Improved dietary fat quality, achieved by replacing SFA with unsaturated fat, reduces LDL-cholesterol and can increase HDL-cholesterol, further improving blood lipid profile. It appears that the effect of combining these interventions is largely additive; however, compliance with multiple changes may reduce over time. Food combinations used in ten ‘portfolio diet’ studies have been reviewed. In clinical efficacy studies of about 1 month where all foods were provided, LDL-cholesterol is reduced by 22–30 %, whereas in community-based studies of >6 months' duration, where dietary advice is the basis of the intervention, reduction in LDL-cholesterol is about 15 %. Inclusion of MUFA into ‘portfolio diets’ increases HDL-cholesterol, in addition to LDL-cholesterol effects. Compliance with some of these dietary changes can be achieved more easily compared with others. By careful food component selection, appropriate to the individual, the effect of including only two components in the diet with good compliance could be a sustainable 10 % reduction in LDL-cholesterol; this is sufficient to make a substantial impact on cholesterol management and reduce the need for pharmaceutical intervention.

HIV-associated lipodystrophy syndrome (HALS), comprising metabolic and morphological alterations, is a known side effect of highly active antiretroviral therapy (HAART). Evidence for the role of nutrition in the management of the systemic parameters of HALS is currently limited. In the present paper we review the current knowledge base surrounding HALS, focusing particularly on the role of nutrition in mitigating the systemic parameters of the syndrome. Reported prevalence of HALS was found to vary from 9 to 83 % due to lack of a standardised definition, as well as variations in assessment methods and in the study population used. HALS is associated with both morphological (lipoatrophy, lipohypertrophy) and metabolic (dyslipidaemia, glucose intolerance, diabetes, hypertension, endothelial dysfunction and atherosclerosis) alterations, which may occur singly or in combination, and are associated with an increased risk of CVD. HAART-induced adipocyte inflammation, oxidative stress and macrophage infiltration, as well as altered adipocyte function and mitochondrial toxicity, have been shown to be central to the development of HALS. The adipocyte, therefore, represents a plausible target for treatment. Pharmacological and surgical treatment interventions have shown effect. However, their use is associated with numerous adverse effects and complications. Targeted lifestyle interventions may provide a useful alternative for managing HALS owing to their safety and tolerability. A Mediterranean-style diet has been found to be effective in improving the systemic parameters of HALS. Furthermore, the effects of n-3 PUFA supplementation are encouraging and future randomised controlled trials investigating the beneficial effects of n-3 PUFA in HALS are justified.

Endothelial dysfunction is a turning point in the initiation and development of atherosclerosis and its complications and is predictive of future cardiovascular events. Ingestion of high-carbohydrate or high-fat meals often results in postprandial hyperglycaemia and/or hypertriacylglycerolaemia that may lead to a transient impairment in endothelial function. The present review will discuss human studies evaluating the impact of high-carbohydrate and high-fat challenges on postprandial endothelial function as well as the potential role of oxidative stress in such postprandial metabolic alterations. Moreover, the present review will differentiate the postprandial endothelial and oxidative impact of meals rich in varying fatty acid types.