Emerging evidence suggests that dietary phytochemicals, in particular flavonoids, may exert beneficial effects on the central nervous system by protecting neurons against stress-induced injury, by suppressing neuroinflammation and by improving cognitive function. It is likely that flavonoids exert such effects, through selective actions on different components of a number of protein kinase and lipid kinase signalling cascades, such as the phosphatidylinositol-3 kinase (PI3K)/Akt, protein kinase C and mitogen-activated protein kinase (MAPK) pathways. This review explores the potential inhibitory or stimulatory actions of flavonoids within these pathways, and describes how such interactions are likely to underlie neurological effects through their ability to affect the activation state of target molecules and/or by modulating gene expression. Future research directions are outlined in relation to the precise site(s) of action of flavonoids within signalling pathways and the sequence of events that allow them to regulate neuronal function.

Recent epidemiological studies in people whose birth weights were recorded many years ago suggest links between impaired growth during early life and the development of diseases, including diabetes, much later in life. The long-term effects of retarded early growth are proposed to result from malnutrition at critical periods of fetal or infant development leading to reduction in the growth of organs and permanent changes in their metabolism or structure, or both. In order to investigate this, a rat model was established which involved feeding either a diet containing 200 g protein/kg or an isoenergetic diet containing 80 g protein/kg to pregnant and lactating rats. In addition, cross-fostering techniques were employed which allowed a separate evaluation of the prenatal or the postnatal periods. The offspring were studied at 21 d of age or were weaned onto a normal laboratory chow and studied at 11 months of age. The 80g protein/kg diet during pregnancy did not affect the overall reproductive performance although more subtle differences were evident. Permanent growth retardation was evident in offspring subjected to maternal protein restriction during the postnatal period. At 21 d of age the offspring of protein-restricted mothers exhibited selective changes in organ growth: compared with the body weight, the lung and brain experienced a smaller decrease in weight; the heart, kidney and thymus decreased proportionately; whereas, the pancreas, spleen, muscle and liver showed a greater reduction in weight. In older animals the muscle weight was lower in the male rats and the relative weight ofpancreas was increased in the female rats.

The aim of the present prospective study was to determine if malnutrition, measured using a simple validated score, is an independent risk factor for nosocomial infections (NI) in non-selected hospital in-patients. Between 29 and 31 May 2001, a survey on the prevalence of NI was conducted on all 1637 in-patients (61 (sd 25) years old) in a French university hospital as part of a national survey. Actual and usual body weights were recorded in all in-patients, and serum albumin levels were measured on all blood samples taken during the week before the study. Nutritional status was evaluated by using the nutritional risk index (NRI). Albumin values were obtained in 1084 patients, and complete weight information was obtained in 911. Therefore, NRI was calculated in 630 patients (61 (sd 20) years old): 427 (67·8%) were malnourished. NI prevalence was 8·7%: 4·4% in non-malnourished patients, 7·6% in moderately malnourished patients and 14·6% in severely malnourished patients. In univariate analysis, the odds ratios for NI were 1·46 (95% CI 1·2, 2·1) in moderately malnourished patients and 4·8 (95% CI 4·6, 6·4) in severely malnourished patients. In multivariate analysis, age, immunodeficiency and NRI class influenced NI risk. Vascular and urinary catheters, and surgical intervention, were the extrinsic factors associated with NI, with odds ratios ranging from 2·0 (95% CI 1·8, 2·6) for vascular catheters to 10·8 (95% CI 8·8, 12·6) for association of the three factors. In conclusion, in non-selected hospitalized patients, malnutrition assessed with a simple and objective marker is an independent risk factor for NI. An early screening for malnutrition may therefore be helpful to reduce the high prevalence of NI.

There is intense interest in the studies related to the potential of phytochemical-rich foods to prevent age-related neurodegeneration and cognitive decline. Recent evidence has indicated that a group of plant-derived compounds known as flavonoids may exert particularly powerful actions on mammalian cognition and may reverse age-related declines in memory and learning. In particular, evidence suggests that foods rich in three specific flavonoid sub-groups, the flavanols, anthocyanins and/or flavanones, possess the greatest potential to act on the cognitive processes. This review will highlight the evidence for the actions of such flavonoids, found most commonly in fruits, such as apples, berries and citrus, on cognitive behaviour and the underlying cellular architecture. Although the precise mechanisms by which these flavonoids act within the brain remain unresolved, the present review focuses on their ability to protect vulnerable neurons and enhance the function of existing neuronal structures, two processes known to be influenced by flavonoids and also known to underpin neuro-cognitive function. Most notably, we discuss their selective interactions with protein kinase and lipid kinase signalling cascades (i.e. phosphoinositide-3 kinase/Akt and mitogen-activated protein kinase pathways), which regulate transcription factors and gene expression involved in both synaptic plasticity and cerebrovascular blood flow. Overall, the review attempts to provide an initial insight into the potential impact of regular flavonoid-rich fruit consumption on normal or abnormal deteriorations in cognitive performance.

In the present study the actual role of propionic acid in the control of fatty acid and cholesterol synthesis was investigated in isolated liver cells from fed rats maintained in the presence of near-physiological concentrations of glucose, glutamine and acetate. Using 3H2O for lipid labelling, propionate appears as an effective inhibitor of fatty acid synthesis and to a lesser extent of cholesterol synthesis, even at the lowest concentration used (0·6 mmol/l). Butyrate is a potent activator of both synthetic pathways, and the activating effect was not counteracted by propionate. Using 1-[14C]acetate, it was observed that propionate at a moderate concentration, or 1 mmol oleate/l, are both very effective inhibitors of 14C incorporation into fatty acid and cholesterol. This incorporation was drastically inhibited when propionate and oleate were present together in the incubation medium. The net utilization of acetate by rat hepatocytes was impaired by propionate, in contrast to oleate. 1-[14C]butyrate was utilized at a high rate for fatty acid synthesis, but to a lesser extent for cholesterol synthesis; both processes were unaffected by propionate. Intracellular citrate concentration was not markedly depressed by propionate, whereas it was strongly elevated by butyrate. In conclusion, propionate may represent an effective inhibitor of lipid synthesis when acetate is a major source of acetyl-CoA, a situation which is encountered with diets rich in readily-fermentable fibres. The present findings also suggest that propionate may be effective at concentrations close to values measured in vivo in the portal vein.

Diet influences the composition of the gut microbiota and host's health, particularly in patients suffering from food-related diseases. Coeliac disease (CD) is a permanent intolerance to cereal gluten proteins and the only therapy for the patients is to adhere to a life-long gluten-free diet (GFD). In the present preliminary study, the effects of a GFD on the composition and immune function of the gut microbiota were analysed in ten healthy subjects (mean age 30·3 years) over 1 month. Faecal microbiota was analysed by fluorescence in situ hybridisation (FISH) and quantitative PCR (qPCR). The ability of faecal bacteria to stimulate cytokine production by peripheral blood mononuclear cells (PBMC) was determined by ELISA. No significant differences in dietary intake were found before and after the GFD except for reductions (P = 0·001) in polysaccharides. Bifidobacterium, Clostridium lituseburense and Faecalibacterium prausnitzii proportions decreased (P = 0·007, P = 0·031 and P = 0·009, respectively) as a result of the GFD analysed by FISH. Bifidobacterium, Lactobacillus and Bifidobacterium longum counts decreased (P = 0·020, P = 0·001 and P = 0·017, respectively), while Enterobacteriaceae and Escherichia coli counts increased (P = 0·005 and P = 0·003) after the GFD assessed by qPCR. TNF-α, interferon-γ, IL-10 and IL-8 production by PBMC stimulated with faecal samples was also reduced (P = 0·021, P = 0·037, P = 0·002 and P = 0·007, respectively) after the diet. Therefore, the GFD led to reductions in beneficial gut bacteria populations and the ability of faecal samples to stimulate the host's immunity. Thus, the GFD may constitute an environmental variable to be considered in treated CD patients for its possible effects on gut health.

Colorectal cancer (CRC) is a leading cause of preventable cancer deaths worldwide, with dietary factors being recognised as key risk modifiers. Foods containing dietary fibre are protective to a degree that the World Cancer Research Fund classifies the evidence supporting their consumption as ‘convincing’. The mechanisms by which fibre components protect against CRC remain poorly understood, especially their interactions with the gut microbiome. Fibre is a composite of indigestible plant polysaccharides and it is emerging that fermentable fibres, including resistant starch (RS), are particularly important. RS fermentation induces SCFA production, in particular, relatively high butyrate levels, and in vitro studies have shown that this acid has strong anti-tumorigenic properties. Butyrate inhibits proliferation and induces apoptosis of CRC cell lines at physiological concentrations. These effects are attributed to butyrate's ability to alter gene transcription by inhibiting histone deacetylase activity. However, the more recent discovery of G-protein coupled receptors that bind butyrate and other SCFA and data obtained from proteomic and genomic experiments suggest that alternative pathways are involved. Here, we review the mechanisms involved in butyrate-induced apoptosis in CRC cells and, additionally, the potential role this SCFA may play in mediating key processes in tumorigenesis including genomic instability, inflammation and cell energy metabolism. This discussion may help to inform the development of strategies to lower CRC risk at the individual and population levels.

Dietary incorporation of fermentable, indigestible fructans may be of benefit to gastrointestinal health by providing short-chain fatty acids, stimulating the proliferation of bifidobacteria or lactobacilli and suppressing potential pathogenic organisms in the gut. We tested the hypothesis that the effects of fructans on caecal, colonic and faecal short-chain fatty acid concentration and microflora composition depend on their chain length. Germ-free rats associated with a human faecal flora were randomly assigned to one of four treatments as follows: (1) commercial standard diet as a control (Con); (2) Con+50 g short-chain oligofructose/kg (OF); (3) C+50 g long-chain inulin/kg (lcIN); or (4) Con+50 g OF–lcIN/kg (Mix OF–lcIN). Changes in bacterial population groups in response to feeding these diets were investigated with 16S rRNA-targeted probes applied in in situ hybridization. Mix OF–lcIN- and lcIN-containing diets resulted in larger numbers of caecal, colonic and faecal bacteria of the Clostridium coccoides–Eubacterium rectale cluster than Con (10·6 and 10·3 v. 9·5 log10/g wet wt), whereas OF alone did not affect this bacterial group in caecum, colon or faeces. A bifidogenic effect was only observed in the colon and faeces of OF-treated rats. More lactobacilli were found in caecal and colonic contents of Mix OF–lcIN-fed rats and in faeces of OF-fed rats compared with Con. Mix OF–lcIN and OF led to significantly smaller numbers of caecal, colonic and faecal bacteria belonging to the Clostridium histolyticum and C. lituseburense groups than Con (6·8 and 6·9 v. 7·9 log10/g wet wt). Counts of total bacteria, Bacteroides–Prevotella and Enterobacteriaceae did not differ between the groups. OF and/or lcIN-containing diets significantly increased the caecal and colonic concentration of butyrate and its relative molar proportion. Only lcIN-containing diets resulted in a higher faecal concentration of butyrate than Con. Higher molar proportions of faecal butyrate were observed with all diets that had been supplemented with OF and/or lcIN. Stimulation of butyrate production could be of interest for the prevention of ulcerative colitis and colon cancer.

Oxidative stress is involved in the development of many chronic diseases. One of the main factors involved in oxidative stress reduction is increased antioxidant potential. Some nutrients such as vitamin C, vitamin E and carotenoids are known to act as antioxidants; however, riboflavin is one of the neglected antioxidant nutrients that may have an antioxidant action independently or as a component of the glutathione redox cycle. Herein, studies that have examined the antioxidant properties of riboflavin and its effect on oxidative stress reduction are reviewed. The results of the reviewed studies confirm the antioxidant nature of riboflavin and indicate that this vitamin can protect the body against oxidative stress, especially lipid peroxidation and reperfusion oxidative injury. The mechanisms by which riboflavin protects the body against oxidative stress may be attributed to the glutathione redox cycle and also to other possible mechanisms such as the conversion of reduced riboflavin to the oxidised form.

1. The inclusion of phytate (10 g/kg) in a purified diet containing zinc (15 mg/kg) fed to young male rats significantly reduced growth rate and food intake, and promoted a cyclic pattern of food intake characteristic of an uncomplicated Zn deficiency. The decreased growth rate could be accounted for by the reduced food consumption.

2. Rats maintained on a Zn-deficient diet (0.5 mg Zn/kg) were found to have a cyclic pattern of food intake and a very slight weight gain. The addition of phytate (10 g/kg) to the Zn-deficient diet promoted a net loss of mean body-weight.

3. Rats maintained on the Zn-supplemented diet containing phytate excreted significantly more Zn in their faeces than either pair-fed or ad lib.-fed control rats. Rats given the Zn-deficient diet supplemented with phytate excreted more Zn in their faeces than Zn-deficient control rats.

4. Dietary phytate significantly reduced the average daily accumulation (μg/d) and wholebody retention (relative to dietary intake) of iron, copper, manganese and Zn, whether or not the diet was supplemented with Zn.

5. The addition of phytate to the lumen fluid of ligated loops of rat duodenum maintained in situ significantly inhibited 65Zn absorption, compared with the control systems without added phytate.

6. Other studies using ligated duodenal and ileal loops indicated that Zn is secreted into the gut lumen and approximately one-third of this is normally reabsorbed. Recycling of endogenous Zn may be a significant process in the over-all body economy of this trace element.

7. The absorption of 65Zn added to the diet was significantly reduced by dietary phytate. Dietary phytate also reduced the biological half-life of body 65Zn from 91 to 211 h post-administration, possibly by inhibiting reabsorption of endogenous 65Zn and thus promoting a more rapid loss from the body.

The Tanita body-fat analyser is a novel device to estimate body fat, based on the principles of bioelectrical impedance. It differs from other impedance systems which use surface electrodes in that the subjects stand bare-footed on a metal sole-plate which incorporates the electrodes, hence impedance is measured through the legs and lower trunk. In 104 men and 101 women (16–78 years and BMI 16–41 kg/m2) the mean bias in body-fat mass measured using the Tanita body-fat analyser was 0·8 (2SD 7·9) KG RELATIVE TO A FOUR-COMPARTMENT MODEL. THIS IS COMPARABLE TO THE OTHER PREDICTION TECHNIQUES TESTED (CONVENTIONAL TETRAPOLAR IMPEDANCE -1·3 (2sd 6·9) kg, skinfold thicknesses 0·3 (2sd 7·4) kg, and BMI-based formulas -0·2 (2sd 9·0) kg and -0·6 (2sd 8·5) kg), but the agreement was poorer than for ‘reference’ methods to measure body fat (density 0·2 (2sd 3·7) kg, total body water -0·9 (2sd 3·4) kg and dual-energy X-ray absorptiometry 0·1 (2sd 5·0) kg). The present paper also describes the derivation of a new prediction equation for the calculation of body composition from the Tanita body-fat analyser. The equation incorporates sex, age, and a log-transformation of height, weight and the measured impedance to predict body fat measured by a four-compartment model. This approach is recommended in the derivation of other prediction equations in body composition analysis. Using this novel prediction equation the residual standard deviations were 4·8 % for men and 3·3 % for women. A similar analysis using data collected with a conventional tetrapolar system yielded residual standard deviations of 4·3 % for men and 3·1 % for women. This demonstrates that the practical simplicity of the novel Tanita method is not associated with a clinically significant decrement in performance relative to a traditional impedance device.

The relationship between omega-3 polyunsaturated fatty acids (n-3 PUFA) from seafood sources (eicosapentaenoic acid, EPA; docosahexaenoic acid, DHA) or plant sources (alpha-linolenic acid, ALA) and risk of type 2 diabetes mellitus (DM) remains unclear. We systematically searched multiple literature databases through June 2011 to identify prospective studies examining relations of dietary n-3 PUFA, dietary fish and/or seafood, and circulating n-3 PUFA biomarkers with incidence of DM. Data were independently extracted in duplicate by 2 investigators, including multivariate-adjusted relative risk (RR) estimates and corresponding 95 % CI. Generalized least-squares trend estimation was used to assess dose–response relationships, with pooled summary estimates calculated by both fixed-effect and random-effect models. From 288 identified abstracts, 16 studies met inclusion criteria, including 18 separate cohorts comprising 540 184 individuals and 25 670 cases of incident DM. Consumption of fish and/or seafood was not significantly associated with DM (n = 13 studies; RR per 100 g/d = 1·12, 95 % CI = 0·94, 1·34); nor were consumption of EPA+DHA (n = 16 cohorts; RR per 250 mg/d = 1·04, 95 % CI = 0·97, 1·10) nor circulating levels of EPA+DHA biomarkers (n = 5 cohorts; RR per 3 % of total fatty acids = 0·94, 95 % CI = 0·75, 1·17). Both dietary ALA (n = 7 studies; RR per 0·5 g/d = 0·93, 95 % CI = 0·83, 1·04) and circulating ALA biomarker levels (n = 6 studies; RR per 0·1 % of total fatty acid = 0·90, 95 % CI = 0·80, 1·00, P = 0·06) were associated with non-significant trend towards lower risk of DM. Substantial heterogeneity (I2~80 %) was observed among studies of fish/seafood or EPA+DHA and DM; moderate heterogeneity ( < 55 %) was seen for dietary and biomarker ALA and DM. In unadjusted meta-regressions, study location (Asia vs. North America/Europe), mean BMI, and duration of follow-up each modified the association between fish/seafood and EPA+DHA consumption and DM risk (P-interaction ≤ 0·02 each). We had limited statistical power to determine the independent effect of these sources of heterogeneity due to their high collinearity. The overall pooled findings do not support either major harms or benefits of fish/seafood or EPA+DHA on development of DM, and suggest that ALA may be associated with modestly lower risk. Reasons for potential heterogeneity of effects, which could include true biologic heterogeneity, publication bias, or chance, deserve further investigation.

The aim of the present study was to assess the reliability, comparative validity and stability of dietary patterns defined by factor analysis for participants of the Tehran Lipid and Glucose Study. A total of 132 subjects, aged ≥ 20 years, completed a 168-item FFQ (FFQ1, FFQ2) twice, with a 14-month interval. Over this duration, twelve dietary recalls (DR) were collected each month. To assess the stability of the FFQ, participants completed the third FFQ (FFQ3) after 8 years. Following these, two dietary patterns – the ‘Iranian Traditional’ and the ‘Western’ – were derived from FFQ1 and FFQ2 and the mean of DR (mDR); and three dietary patterns were identified from FFQ3: the ‘Iranian Traditional’, the ‘Western’ and the ‘Combined’. The reliability correlations between factor scores of the two FFQ were 0·72 for the Iranian Traditional and 0·80 for the Western pattern; corrected month-to-month variations of DR correlations between the FFQ2 and mDR were 0·48 for the first and 0·75 for the second pattern. The 95 % limits of agreement for the difference between factor scores obtained from FFQ2 and mDR lay between − 1·58 and +1·58 for the Iranian Traditional and between − 1·33 and +1·33 for the Western pattern. The intra-class correlations between FFQ2 and FFQ3 were − 0·09 (P = 0·653) and 0·49 (P <0·001) for the ‘Iranian Traditional’ and the ‘Western’, respectively. These data indicate reasonable reliability and validity of the dietary patterns defined by factor analysis. Although the Western pattern was found to be fairly stable, the Iranian Traditional pattern was mostly unstable over the 8 years of the study period.

In clinical practice and epidemiological surveys, anthropometric measurements represent an important component of nutritional assessment in the elderly. The anthropometric standards derived from adult populations may not be appropriate for the elderly because of body composition changes occurring during ageing. Specific anthropometric reference data for the elderly are necessary. In the present study we investigated anthropometric characteristics and their relationship to gender and age in a cross-sectional sample of 3356 subjects, randomly selected from an elderly Italian population. In both sexes, weight and height significantly decreased with age while knee height did not. The BMI was significantly higher in women than in men (27·6 SD 5·7 V. 26·4 sd 3·7; P<0·001) and it was lower in the oldest than in the youngest subjects (P<0·05) of both genders. The 75th year of age was a turning point for BMI as for other anthropometric measurements. According to BMI values, the prevalence of malnutrition was lower than 5 % in both genders, whereas obesity was shown to have a higher prevalence in women than in men (28 % v. 16 %; P<0·001). Waist circumference and waist : hip ratio values were higher for the youngest men than for the oldest men (P<0·05), whereas in women the waist : hip ratio values were higher in the oldest women, suggesting that visceral redistribution in old age predominantly affects females. In conclusion, in the elderly the oldest subjects showed a thinner body frame than the youngest of both genders, and there was a more marked fat redistribution in women.

Balanced glucose metabolism ensures optimal fetal growth with long-term health implications conferred on both mother and child. We examined whether supplementation of probiotics with dietary counselling affects glucose metabolism in normoglycaemic pregnant women. At the first trimester of pregnancy 256 women were randomised to receive nutrition counselling to modify dietary intake according to current recommendations or as controls; the dietary intervention group was further randomised to receive probiotics (Lactobacillus rhamnosus GG and Bifidobacterium lactis Bb12; diet/probiotics) or placebo (diet/placebo) in a double-blind manner, whilst the control group received placebo (control/placebo). Blood glucose concentrations were lowest in the diet/probiotics group during pregnancy (baseline-adjusted means 4·45, 4·60 and 4·56 mmol/l in diet/probiotics, diet/placebo and control/placebo, respectively; P = 0·025) and over the 12 months' postpartum period (baseline-adjusted means 4·87, 5·01 and 5·02 mmol/l; P = 0·025). Better glucose tolerance in the diet/probiotics group was confirmed by a reduced risk of elevated glucose concentration compared with the control/placebo group (OR 0·31 (95 % CI 0·12, 0·78); P = 0·013) as well as by the lowest insulin concentration (adjusted means 7·55, 9·32 and 9·27 mU/l; P = 0·032) and homeostasis model assessment (adjusted means 1·49, 1·90 and 1·88; P = 0·028) and the highest quantitative insulin sensitivity check index (adjusted means 0·37, 0·35 and 0·35; P = 0·028) during the last trimester of pregnancy. The effects observed extended over the 12-month postpartum period. The present study demonstrated that improved blood glucose control can be achieved by dietary counselling with probiotics even in a normoglycaemic population and thus may provide potential novel means for the prophylactic and therapeutic management of glucose disorders.

There is a consensus that interventions to prevent and treat childhood obesity should involve the family; however, the extent of the child's involvement has received little attention. The goal of the present study was to evaluate the relative efficacy of treating childhood obesity via a family-based health-centred intervention, targeting parents alone v. parents and obese children together. Thirty-two families with obese children of 6–11 years of age were randomised into groups, in which participants were provided for 6 months a comprehensive educational and behavioural programme for a healthy lifestyle. These groups differed in their main agent of change: parents-only v. the parents and the obese child. In both groups, parents were encouraged to foster authoritative parenting styles (parents are both firm and supportive; assume a leadership role in the environmental change with appropriate granting of child's autonomy). Only the intervention aimed at parents-only resulted in a significant reduction in the percentage overweight at the end of the programme (P=0·02) as well as at the 1-year follow-up meeting.The differences between groups at both times were significant (P<0·05). A greater reduction in food stimuli in the home (P<0·05) was noted in the parents-only group. In both groups, the parents' weight status did not change. Regression analysis shows that the level of attendance in sessions explained 28% of the variability in the children's weight status change, the treatment group explained another 10%, and the improvement in the obesogenic load explained 11% of the variability. These results suggest that omittingthe obese child from active participation in the health-centred programme may be beneficial for weight loss and for the promotion of a healthy lifestyle among obese children.

Rats were fed a grape seed extract (GSE) containing (+)-catechin, (−)-epicatechin and dimers, trimers, tetramers and polymeric procyanidins. Liver, kidney, brain and gastrointestinal (GI) tract together with plasma, urine and faeces were collected over a 24 h period and their flavan-3-ol content was analysed by HPLC with tandem mass spectrometry and diode array detection. Small amounts of the GSE flavan-3-ols moved out of the stomach and into the duodenum/jejunum, and to a greater extent the ileum 1 h after ingestion, and into the caecum after 2 h with relatively small amounts being detected in the colon after 3 h. The GI tract contained the parent GSE flavan-3-ols and procyanidins with only trace amounts of metabolites and there were no indications that proanthocyanidins were depolymerised in the GI tract releasing monomeric flavan-3-ols. Plasma contained exclusively catechin glucuronides and methylated glucuronide metabolites which were also detected in the liver and kidneys. These metabolites were also present in urine together with sulphated metabolites and low amounts of the procyanidin dimers B1, B2, B3 and B4 as well as the trimer C2 and an unknown GSE trimer. The amounts of (+)-catechin and (−)-epicatechin metabolites excreted in urine relative to the quantity of the monomers ingested were 27 and 36 %, respectively, after 24 h. This is similar to the levels of urinary excretion reported to occur by other investigators after feeding (−)-epicatechin to rats and provides further, albeit indirect, evidence that the procyanidin oligomers in the GSE were not depolymerised to monomers to any extent after ingestion. No convincing analytical data were obtained for the presence of flavan-3-ol metabolites in the brain.

Most of diurnal time is spent in a postprandial state due to successive meal intakes during the day. As long as the meals contain enough fat, a transient increase in triacylglycerolaemia and a change in lipoprotein pattern occurs. The extent and kinetics of such postprandial changes are highly variable and are modulated by numerous factors. This review focuses on factors affecting postprandial lipoprotein metabolism and genes, their variability and their relationship with intermediate phenotypes and risk of CHD. Postprandial lipoprotein metabolism is modulated by background dietary pattern as well as meal composition (fat amount and type, carbohydrate, protein, fibre, alcohol) and several lifestyle conditions (physical activity, tobacco use), physiological factors (age, gender, menopausal status) and pathological conditions (obesity, insulin resistance, diabetes mellitus). The roles of many genes have been explored in order to establish the possible implications of their variability in lipid metabolism and CHD risk. The postprandial lipid response has been shown to be modified by polymorphisms within the genes for apo A-I, A-IV, A-V, E, B, C-I and C-III, lipoprotein lipase, hepatic lipase, fatty acid binding and transport proteins, microsomal triglyceride transfer protein and scavenger receptor class B type I. Overall, the variability in postprandial response is important and complex, and the interactions between nutrients or dietary or meal compositions and gene variants need further investigation. The extent of present knowledge and needs for future studies are discussed in light of ongoing developments in nutrigenetics.