The position of fatty acids in the TAG molecule (sn-1, sn-2 and sn-3) determines the physical properties of the fat, which affects its absorption, metabolism and distribution into tissues, which may have implications for the risk of CHD. The TAG structure of fats can be manipulated by the process of interesterification, which is of increasing commercial importance, as it can be used to change the physical characteristics of a fat without the generation of trans-fatty acids. Interesterified fats rich in long-chain SFA are commercially important, but few studies have investigated their health effects. Evidence from animal and human infant studies suggests that TAG structure and interesterification affect digestibility, atherogenicity and fasting lipid levels, with fats containing palmitic and stearic acid in the sn-2 position being better digested and considered to be more atherogenic. However, chronic studies in human adults suggest that TAG structure has no effect on digestibility or fasting lipids. The postprandial effects of fats with differing TAG structure are better characterised but the evidence is inconclusive; it is probable that differences in the physical characteristics of fats resulting from interesterification and changes in TAG structure are key determinants of the level of postprandial lipaemia, rather than the position of fatty acids in the TAG. The present review gives an overview of TAG structure and interesterified palmitic and stearic acid-rich fats, their physical properties and their acute and chronic effects in human adults in relation to CHD.

Obesity is a multi-faceted disease, predisposing sufferers to numerous co-morbidities such as epithelial dysfunction and insulin resistance which ultimately result in CVD. Visceral adipose tissue in particular is associated with inflammation due to the release of pro-inflammatory cytokines by adipocytes. Inflammation seems to be rather central in causing damage to endothelial cells as well as exerting negative effects on glucose metabolism, ultimately leading to insulin resistance. Resveratrol is a naturally occurring phenolic substance which has been found to display anti-inflammatory, vasoprotective and insulin-sensitising effects, among others. The popularity of resveratrol use is escalating in the treatment of various ailments including obesity in adults. The use of the substance in childhood obesity is, however, a worrying factor, as no studies have as yet been performed on adolescent animals and there is evidence of kidney toxicity of resveratrol and its metabolites at intake levels below those currently approved as safe. Another cause for concern is the uncertainty surrounding long-term, low-dose administration of the substance in humans. The supplement should thus not be recommended for use in the prevention and treatment of obesity until conclusive research is established on the safety of long-term usage of resveratrol in both children and adults.

Vitamin D is unique among the vitamins in that man can synthesise it via the action of UV radiation upon the skin. This combined with its ability to act on specific target tissues via vitamin D receptors (VDR) make its classification as a steroid hormone more appropriate. While vitamin D deficiency is a recognised problem in some northern latitude countries, recent studies have shown that even in sunny countries, such as Australia, vitamin D deficiency may be more prevalent than first thought. Vitamin D is most well known for its role in bone health; however, the discovery of VDR on a wide variety of tissue types has also opened up roles for vitamin D far beyond traditional bone health. These include possible associations with autoimmune diseases such as multiple sclerosis and inflammatory bowel diseases, cancer, CVD and muscle strength. First, this paper presents an overview of the two sources of vitamin D: exposure to UVB radiation and food sources of vitamin D, with particular focus on both Australian and international studies on dietary vitamin D intake and national fortification strategies. Second, the paper reviews recent epidemiological and experimental evidence linking vitamin D and its role in health and disease for the major conditions linked to suboptimal vitamin D, while identifying significant gaps in the research and possible future directions for research.

The amount and type of dietary fat have long been associated with the risk of CVD. Arterial stiffness and endothelial dysfunction are important risk factors in the aetiology of CHD. A range of methods exists to assess vascular function that may be used in nutritional science, including clinic and ambulatory blood pressure monitoring, pulse wave analysis, pulse wave velocity, flow-mediated dilatation and venous occlusion plethysmography. The present review focuses on the quantity and type of dietary fat and effects on blood pressure, arterial compliance and endothelial function. Concerning fat quantity, the amount of dietary fat consumed habitually appears to have little influence on vascular function independent of fatty acid composition, although single high-fat meals postprandially impair endothelial function compared with low-fat meals. The mechanism is related to increased circulating lipoproteins and NEFA which may induce pro-inflammatory pathways and increase oxidative stress. Regarding the type of fat, cross-sectional data suggest that saturated fat adversely affects vascular function whereas polyunsaturated fat (mainly linoleic acid (18 : 2n-6) and n-3 PUFA) are beneficial. EPA (20 : 5n-3) and DHA (22 : 6n-3) can reduce blood pressure, improve arterial compliance in type 2 diabetics and dyslipidaemics, and augment endothelium-dependent vasodilation. The mechanisms for this vascular protection, and the nature of the separate physiological effects induced by EPA and DHA, are priorities for future research. Since good-quality observational or interventional data on dietary fatty acid composition and vascular function are scarce, no further recommendations can be suggested in addition to current guidelines at the present time.

In order to determine the impact of garlic on total cholesterol (TC), TAG levels, as well as LDL and HDL, and establish if any variables have an impact on the magnitude of this effect, a meta-analysis was conducted. A systematic literature search of MEDLINE, CINAHL and the Cochrane Database from the earliest possible date through to November 2007 was conducted to identify randomised, placebo-controlled trials of garlic that reported effects on TC, TAG concentrations, LDL or HDL. The weighted mean difference of the change from baseline (with 95 % CI) was calculated as the difference between the means in the garlic groups and the control groups using a random-effects model. Subgroup and sensitivity analyses were performed to determine the effects on type, brand and duration of garlic therapy as well as baseline TC and TAG levels, the use of dietary modification, and study quality on the meta-analysis's conclusions. Twenty-nine trials were included in the analysis. Upon meta-analysis garlic was found to significantly reduce TC ( − 0·19; 95 % CI − 0·33, − 0·06 mmol/l) and TAG ( − 0·11; 95 % CI − 0·19, − 0·06 mmol/l) but exhibited no significant effect on LDL or HDL. There was a moderate degree of statistical heterogeneity for the TC and TAG analyses. Garlic reduces TC to a modest extent, an effect driven mostly by the modest reductions in TAG, without appreciable LDL lowering or HDL elevation. Higher baseline line TC levels and the use of dietary modification may alter the effect of garlic on these parameters. Future studies should be conducted evaluating the impact of adjunctive garlic therapy with fibrates or statins on TAG concentrations.

Research conducted among adults has mainly shown that visceral adipose tissue (VAT) is strongly linked to insulin resistance, type 2 diabetes, hypertension and dyslipidaemia, leading to increased risk of CVD or the metabolic syndrome. However, little is known about the aetiology, determinants and consequences of VAT in children. The present article reviews the current literature relating to the factors influencing visceral fat accumulation in children and adolescents. The literature used in the present study was collected by searching a PubMed database, in which studies up to 2008 exploring the factors influencing accumulation of visceral fat among children and youth were found on the basis of appropriate keywords. Further studies concerning different factors influencing deposition of VAT among children and youth should first of all concentrate on: carrying out long-term analyses among children of different ethnical groups, which should begin in the period of prepuberty and which should cover the whole period of puberty till adulthood; drawing up norms specifying the amount of VAT among healthy children; identification of anthropometric indicators which will help to determine the VAT:subcutaneous adipose tissue ratio in the most precise way; broader studies of the influence of eating habits on developing VAT deposit among children and youth.

In the present review concerning stroke, we evaluate the roles of B vitamins, homocysteine and antioxidant vitamins. Stroke is a leading cause of death in developed countries. However, current therapeutic strategies for stroke have been largely unsuccessful. Several studies have reported important benefits on reducing the risk of stroke and improving the post-stroke-associated functional declines in patients who ate foods rich in micronutrients, including B vitamins and antioxidant vitamins E and C. Folic acid, vitamin B6 and vitamin B12 are all cofactors in homocysteine metabolism. Growing interest has been paid to hyperhomocysteinaemia as a risk factor for CVD. Hyperhomocysteinaemia has been linked to inadequate intake of vitamins, particularly to B-group vitamins and therefore may be amenable to nutritional intervention. Hence, poor dietary intake of folate, vitamin B6 and vitamin B12 are associated with increased risk of stroke. Elevated consumption of fruits and vegetables appears to protect against stroke. Antioxidant nutrients have important roles in cell function and have been implicated in processes associated with ageing, including vascular, inflammatory and neurological damage. Plasma vitamin E and C concentrations may serve as a biological marker of lifestyle or other factors associated with reduced stroke risk and may be useful in identifying those at high risk of stroke. After reviewing the observational and intervention studies, there is an incomplete understanding of mechanisms and some conflicting findings; therefore the available evidence is insufficient to recommend the routine use of B vitamins, vitamin E and vitamin C for the prevention of stroke. A better understanding of mechanisms, along with well-designed controlled clinical trials will allow further progress in this area.

Alcohol intake at levels posing an acute heath risk is common amongst teenagers. Alcohol abuse is the second most common mental disorder worldwide. The incidence of smoking is decreasing in the Western world but increasing in developing countries and is the leading cause of preventable death worldwide. Considering the longstanding history of alcohol and tobacco consumption in human societies, it might be surprising that the molecular mechanisms underlying alcohol and smoking dependence are still incompletely understood. Effective treatments against the risk of relapse are lacking. Drugs of abuse exert their effect manipulating the dopaminergic mesocorticolimbic system. In this brain region, alcohol has many potential targets including membranes and several ion channels, while other drugs, for example nicotine, act via specific receptors or binding proteins. Repeated consumption of drugs of abuse mediates adaptive changes within this region, resulting in addiction. The high incidence of alcohol and nicotine co-abuse complicates analysis of the molecular basis of the disease. Gene expression profiling is a useful approach to explore novel drug targets in the brain. Several groups have utilised this technology to reveal drug-sensitive pathways in the mesocorticolimbic system of animal models and in human subjects. These studies are the focus of the present review.

Ca is not only essential for bone mineralisation, but also for regulation of extracellular and intracellular processes. When the Ca2+ intake is low, the efficiency of intestinal Ca2+ absorption and renal Ca2+ reabsorption is increased. This adaptive mechanism involves calcitriol enhancement via parathyroid hormone stimulation. Bone is also highly affected. Low Ca2+ intake is considered a risk factor for osteoporosis. Patients with renal lithiasis may be at higher risk of recurrence of stone formation when they have low Ca2+ intake. The role of dietary Ca2+ on the regulation of lipid metabolism and lipogenic genes in adipocytes might explain an inverse relationship between dairy intake and BMI. Dietary Ca2+ restriction produces impairment of the adipocyte apoptosis and dysregulation of glucocorticosteroid metabolism in the adipose tissue. An inverse relationship between hypertension and a low-Ca2+ diet has been described. Ca2+ facilitates weight loss and stimulates insulin sensitivity, which contributes to the decrease in the blood pressure. There is also evidence that dietary Ca2+ is associated with colorectal cancer. Dietary Ca2+ could alter the ratio of faecal bile acids, reducing the cytotoxicity of faecal water, or it could activate Ca2+-sensing receptors, triggering intracellular signalling pathways. Also it could bind luminal antigens, transporting them into mucosal mononuclear cells as a mechanism of immunosurveillance and promotion of tolerance. Data relative to nutritional Ca2+ and incidences of other human cancers are controversial. Health professionals should be aware of these nutritional complications and reinforce the dairy intakes to ensure the recommended Ca2+ requirements and prevent diseases.

Recent research has provided insights into dietary components that may optimise bone health and stimulate bone formation. Fruit and vegetable intake, as well as grains and other plant-derived food, have been linked to decreased risk of major chronic diseases including osteoporosis. This effect has been partially attributed to the polyphenols found in these foods. Thus, it has been suggested that these compounds may provide desirable bone health benefits through an action on bone cell metabolism. The present review will focus on how some polyphenols can modulate osteoblast function and reports which cellular signalling pathways are potentially implicated. However, to date, despite numerous investigations, few studies have provided clear evidence that phenolic compounds can act on osteoblasts. Polyphenols cited in the present review seem to be able to modulate the expression of transcription factors such as runt-related transcription factor-2 (Runx2) and Osterix, NF-κB and activator protein-1 (AP-1). It appears that polyphenols may act on cellular signalling such as mitogen-activated protein kinase (MAPK), bone morphogenetic protein (BMP), oestrogen receptor and osteoprotegerin/receptor activator of NF-κB ligand (OPG/RANKL) and thus may affect osteoblast functions. However, it is also important to take in account the possible interaction of these compounds on osteoclast metabolism to better understand the positive correlation reported between the consumption of fruit and vegetables and bone mass.

The gastrointestinal tract (GIT) is a metabolically significant site of sulfur amino acid (SAA) metabolism in the body and metabolises about 20 % of the dietary methionine intake which is mainly transmethylated to homocysteine and trans-sulfurated to cysteine. The GIT accounts for about 25 % of the whole-body transmethylation and trans-sulfuration. In addition, in vivo studies in young pigs indicate that the GIT is a site of net homocysteine release and thus may contribute to the homocysteinaemia. The gut also utilises 25 % of the dietary cysteine intake and the cysteine uptake by the gut represents about 65 % of the splanchnic first-pass uptake. Moreover, we recently showed that SAA deficiency significantly suppresses intestinal mucosal growth and reduces intestinal epithelial cell proliferation, and increases intestinal oxidant stress in piglets. These recent findings indicate that intestinal metabolism of dietary methionine and cysteine is nutritionally important for intestinal mucosal growth. Besides their role in protein synthesis, methionine and cysteine are precursors of important molecules. S-adenosylmethionine, a metabolite of methionine, is the principal biological methyl donor in mammalian cells and a precursor for polyamine synthesis. Cysteine is the rate-limiting amino acid for glutathione synthesis, the major cellular antioxidant in mammals. Further studies are warranted to establish how SAA metabolism regulates gut growth and intestinal function, and contributes to the development of gastrointestinal diseases. The present review discusses the evidence of SAA metabolism in the GIT and its functional and nutritional importance in gut function and diseases.

The growing incidence of prediabetes and clinical type 2 diabetes, in part characterised by insulin resistance, is a critical health problem with consequent devastating personal and health-care costs. Vitamin D status, assessed by serum 25-hydroxyvitamin D levels, is inversely associated with diabetes in epidemiological studies. Several clinical intervention studies also support that vitamin D, or its active metabolite 1,25-dihydroxyvitamin D (1,25(OH)2D), improves insulin sensitivity, even in subjects with glucose metabolism parameters classified within normal ranges. The mechanisms proposed which may underlie this effect include potential relationships with improvements in lean mass, regulation of insulin release, altered insulin receptor expression and specific effects on insulin action. These actions may be mediated by systemic or local production of 1,25(OH)2D or by suppression of parathyroid hormone, which may function to negatively affect insulin sensitivity. Thus, substantial evidence supports a relationship between vitamin D status and insulin sensitivity; however, the underlying mechanisms require further exploration.

Overweight and obesity are associated with increased morbidity and mortality, although the range of body weights that is optimal for health is controversial. It is less clear whether weight loss benefits longevity and hence whether weight reduction is justified as a prime goal for all individuals who are overweight (normally defined as BMI>25 kg/m2). The purpose of the present review was to examine the evidence base for recommending weight loss by diet and lifestyle change as a means of prolonging life. An electronic search identified twenty-six eligible prospective studies that monitored subsequent mortality risk following weight loss by lifestyle change, published up to 2008. Data were extracted and further analysed by meta-analysis, giving particular attention to the influence of confounders. Moderator variables such as reason for weight loss (intentional, unintentional), baseline health status (healthy, unhealthy), baseline BMI (normal, overweight, obese), method used to estimate weight loss (measured weight loss, reported weight loss) and whether models adjusted for physical activity (adjusted data, unadjusted data) were used to classify subgroups for separate analysis. Intentional weight loss per se had a neutral effect on all-cause mortality (relative risk (RR) 1·01; P = 0·89), while weight loss which was unintentional or ill-defined was associated with excess risk of 22 to 39 %. Intentional weight loss had a small benefit for individuals classified as unhealthy (with obesity-related risk factors) (RR 0·87 (95 % CI 0·77, 0·99); P = 0·028), especially unhealthy obese (RR 0·84 (95 % CI 0·73, 0·97); P = 0·018), but appeared to be associated with slightly increased mortality for healthy individuals (RR 1·11 (95 % CI 1·00, 1·22); P = 0·05), and for those who were overweight but not obese (RR 1·09 (95 % CI 1·02, 1·17); P = 0·008). There was no evidence for weight loss conferring either benefit or risk among healthy obese. In conclusion, the available evidence does not support solely advising overweight or obese individuals who are otherwise healthy to lose weight as a means of prolonging life. Other aspects of a healthy lifestyle, especially exercise and dietary quality, should be considered. However, well-designed intervention studies are needed clearly to disentangle the influence of physical activity, diet strategy and body composition, in order to define appropriate advice to those populations that might be expected to benefit.

Results from ecological, case–control and cohort studies have shown that vitamin D reduces the risk of bone fracture, falls, autoimmune diseases, type 2 diabetes, CVD and cancer. However, there is still epidemic vitamin D insufficiency especially among individuals living at high latitudes or with dark skin. Serum levels of 25-hydroxyvitamin D (25(OH)D) are considered the best biomarker of vitamin D nutritional status. Appropriate sunshine exposure or oral supplementation is necessary to maintain sufficient vitamin D status, which is generally accepted as serum 25(OH)D>75 nmol/l. Immunoassays, especially RIA, have been primarily used to measure serum 25(OH)D while liquid chromatography–MS (LC–MS) is considered the ‘gold standard’. There is significant disparity among the immunoassays, and all immunoassays have considerable bias compared with LC–MS methods. Because of the variations among the results from these different assays, it is necessary that assay-specific reference ranges be established or standardisation of the assays take place. The present review focuses on ecological, case–control, and cohort studies that investigated the role of vitamin D in health and disease. In addition, analytical techniques used in laboratory evaluation of vitamin D nutritional status are also critically reviewed. The majority of the literature included in the present review is selected from that searchable in PubMed up to the end of September 2008.

The growing public concerns over chemical residues in animal-derived foods and threats of antibiotic-resistant bacteria have renewed interest in exploring safer alternatives to chemical feed additives in ruminant livestock. Various bioactive phytochemicals including saponins appear to be potential ‘natural’ alternatives to ‘chemical’ additives in modulating rumen fermentation favourably and animal performance. Saponins are a diverse group of glycosides present in many families of plants. The primary effect of saponins in the rumen appears to be to inhibit the protozoa (defaunation), which might increase the efficiency of microbial protein synthesis and protein flow to the duodenum. Furthermore, saponins may decrease methane production via defaunation and/or directly by decreasing the activities (i.e. rate of methanogenesis or expression of methane-producing genes) and numbers of methanogens. Saponins may also selectively affect specific rumen bacteria and fungi, which may alter the rumen metabolism beneficially or adversely. The ammonia-adsorption and modulation of digesta passage in the rumen by saponins have also been implicated in altering rumen metabolism, but their physiological responses are likely to be negligible compared with microbiological effects. The effects of saponins on rumen fermentation have not been found to be consistent. These discrepancies appear to be related to the chemical structure and dosage of saponins, diet composition, microbial community and adaptation of microbiota to saponins. There is need for systematic research based on chemical structures of saponins, nutrient composition of diets and their effects on rumen microbial ecosystem to obtain consistent results. The present paper reviews and discusses the effects and mode of action of saponins on microbial community and fermentation in the rumen, and ruminant performance.

Breakfast is recommended as part of a healthy diet because it is associated with healthier macro- and micronutrient intakes, BMI and lifestyle. Breakfast is also widely promoted to improve cognitive function and academic performance, leading to the provision of breakfast initiatives by public health bodies. Despite this positive and intuitive perception of cognitive benefits, there has been no systematic review of the evidence. Systematic review methodology was employed to evaluate the effects of breakfast on cognitive performance in well-nourished children and nutritionally at-risk or stunted children. Acute experimental studies, school feeding programmes and studies of habitual breakfast intake are reviewed. Comparisons of breakfast v. no breakfast and breakfasts differing in energy and macronutrient composition are discussed. Included are forty-five studies described in forty-one papers published between 1950 and 2008. The evidence indicates that breakfast consumption is more beneficial than skipping breakfast, but this effect is more apparent in children whose nutritional status is compromised. There is a lack of research comparing breakfast type, precluding recommendations for the size and composition of an optimal breakfast for children's cognitive function. Few studies examined adolescents. Studies of school breakfast programmes suggest that such interventions can have positive effects on academic performance, but this may be in part explained by the increased school attendance that programmes encourage. The present systematic review considers methodological issues in this field and makes recommendations for future research design and policy priorities.