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.

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.

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.

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 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.