The aims of the present study were to evaluate essential fatty acids (EFA) and long-chain PUFA (LCPUFA) status in lactating adolescents and its association with breast milk composition. Healthy nursing adolescents from Rio de Janeiro, Brazil (n 30; 14–19 years; 30–120 d postpartum), exclusively or predominantly breast-feeding, participated in this study. Breast milk and blood samples were collected after overnight fasting. Fatty acid composition of breast milk, erythrocyte membrane (EM) and plasma NEFA were determined by GC. Indices of fatty acid status (mean melting point (MMP); EFA status index; DHA status indices, 22 : 5n-6:22 : 4n-6 and 22 : 6n-3:22 : 5n-6 ratios) were calculated from EM fatty acid composition. Dietary intake of n-3 fatty acids was low when compared with current recommendations for lactating women. MMP was associated with indices of DHA status, some individual fatty acids in EM and years post-menarche and weeks postpartum, suggesting the use of erythrocyte MMP as a possible comprehensive biochemical marker of LCPUFA status in this physiological condition. The DHA status of lactating adolescents and their milk DHA concentrations were similar to the values of Brazilian lactating adults, but lower compared with the values of lactating adults from other countries. Therefore, these lactating adolescents were apparently not disadvantaged, as compared with the Brazilian adults, when EM and breast milk fatty acid composition were considered. In general, PUFA in milk from adolescents presented few associations with their concentrations in plasma NEFA and with maternal status. However, milk DHA was associated with maternal LCPUFA and DHA states.

In spite of their high oxidisability, long-chain n-3 PUFA protect against CVD. Dietary fatty acids modulate the fatty acid composition of lipoproteins involved in atherosclerosis. We thought that if long-chain n-3 PUFA were able to increase NO production by the aorta, then by its antioxidant activity the NO will prevent lipid peroxidation. However, the beneficial effect of NO in vivo on VLDL+LDL oxidation would only be possible if NO could diffuse to their lipidic core. Rats were fed maize oil- or fish oil as menhaden oil- (MO) rich diets for 8 weeks, to study the effects of MO on aortic NO production, NO diffusion into VLDL+LDL, the extent of oxidation in native VLDL+LDL and their oxidisability ex vivo. Aortic NO production and its α-tocopherol content were increased and n-3 PUFA were incorporated into the VLDL+LDL. In spite of the higher peroxidisability and the low α-tocopherol in native VLDL+LDL from rats fed MO, native VLDL+LDL from the two groups shared similar electrophoretic patterns, conjugated dienes, thiobarbituric acid-reactive substances, total antioxidant capacity, and NO diffusibility on VLDL+LDL, indicative of an in vivo protection against oxidation. However, these results do not correlate with the ex vivo oxidisability of VLDL+LDL, as NO is lacking. Thus, the in vivo beneficial effects can be explained by increased α-tocopherol in aorta and by a compensatory effect of NO on VLDL+LDL against the low α-tocopherol levels, which may contribute to the anti-atherogenic properties of fish oil.

After birth, the gastrointestinal (GI) tract undergoes vast structural and functional adaptations to be able to digest mother's milk and later, during the weaning period, solid food. Studies on germ-free animals have shown the role of the gut microbiota for stimulating GI maturation, but which groups are involved is unclear. In the present study, we administered the probiotic bacterium, Lactobacillus plantarum 299v (Lp299v), in the drinking water to pregnant and lactating rat dams until their pups had reached an age of 14 d. It was found that Lp299v colonizing the mothers were also able to colonize the pups, which had an impact on their gut growth and function. The small intestine, pancreas and liver weighed more in the 14 d-old pups born from dams exposed to Lp299v than in the control pups from dams given only water. Furthermore, the Lp299v pups showed decreased gut permeability. Despite a heavier spleen in the Lp299v pups, as compared to the control pups, no significant increase in the acute-phase protein, haptoglobin, was found. In conclusion, the results reported here clearly show that manipulating the maternal microflora by exposing expecting mothers to a Gram-positive, probiotic bacterium prior to parturition and during lactation impacts the gut growth and function in the offspring.

Animal studies suggest that conjugated linoleic acid (CLA) may modulate the immune response, while studies in healthy human subjects have shown little effect and results are controversial. However, the effects of CLA may be more prominent in situations of immune imbalance, such as allergy. We studied the effects of the natural CLA isomer, cis-9, trans-11-CLA, on allergy symptoms and immunological parameters in subjects with birch pollen allergy. In a randomised, placebo-controlled study, forty subjects (20–46 years) with diagnosed birch pollen allergy received 2 g CLA/d in capsules, which contained 65·3 % cis-9, trans-11-CLA and 8·5 % trans-10, cis-12-CLA (n 20), or placebo (high-oleic acid sunflower-seed oil) (n 20) for 12 weeks. The supplementation began 8 weeks before the birch pollen season and continued throughout the season. Allergy symptoms and use of medication were recorded daily. Lymphocyte subsets, cytokine production, immunoglobulins, C-reactive protein, lipid and glucose metabolism and lipid peroxidation were assessed before and after supplementation. The CLA group reported a better overall feeling of wellbeing (P < 0·05) and less sneezing (P < 0·05) during the pollen season. CLA supplementation decreased the in vitro production of TNF-α (P < 0·01), interferon-γ (P < 0·05) and IL-5 (P < 0·05). Total plasma IgE and birch-specific IgE concentrations did not differ between groups, whereas plasma IgA (P < 0·05), granulocyte macrophage colony-stimulating factor (P < 0·05) and eosinophil-derived neurotoxin (P < 0·05) concentrations were lower after CLA supplementation. Urinary excretion of 8-iso-PGF2α, a major F2-isoprostane (P < 0·01), and 15-keto-dihydro-PGF2α, a primary PGF2α metabolite (P < 0·05), increased in the CLA group. The results suggest that cis-9, trans-11-CLA has modest anti-inflammatory effects in allergic subjects.

During atherogenesis, a pathological accumulation of lipids occurs within aortic intimal macrophages through uptake of plasma oxidised LDL (oxLDL). The aim of the present study was to determine whether macrophage uptake of plasma oxLDL and LDL susceptibility to oxidation may be determined by quantity and quality of dietary fat. Twenty healthy young men were subjected to three dietary periods, each lasting 4 weeks. The first was an SFA-enriched diet (38 % fat, 20 % SFA), which was followed by a carbohydrate (CHO)-rich diet (30 % fat, < 10 % SFA, 55 % CHO) or a MUFA olive oil-rich diet (38 % fat, 22 % MUFA) following a randomised cross-over design. After each diet period, LDL particles were oxidised with Cu ions to determine LDL susceptibility to oxidation and subsequently incubated with the U937-macrophage cell line to determine the percentage of uptake of plasma oxLDL. The shift from the MUFA diet to the SFA- or CHO-rich diets reduced the resistance of LDL particles to oxidation, decreasing lag time (P = 0·038) and increasing the propagation rate (P = 0·001). Furthermore, the MUFA-rich diet demonstrated reduced macrophage uptake of plasma oxLDL (P = 0·031) as compared with the SFA-rich diet. Finally, macrophage uptake of plasma oxLDL was correlated (r 0·45; P = 0·040) with total amount of conjugated dienes after LDL oxidation. Our data suggest that a MUFA-rich diet may have favourable effects on cardiovascular risk since it prevents the oxidative modifications of LDL and reduces macrophage uptake of plasma oxLDL.

There is growing evidence that dietary proteins may interfere with lipid metabolism. We therefore examined the effects of feeding obese Zucker rats a single cell protein (SCP) with low ratios of methionine:glycine and lysine:arginine for 6 weeks. SCP feeding reduced the hepatic steatosis and lowered the plasma transaminase levels when compared with casein-fed rats (controls). The fatty acid oxidation was increased in liver mitochondria and peroxisomes, whereas the activities of enzymes involved in lipogenesis and TAG biosynthesis were unaffected. SCP feeding affected the fatty acid composition of liver lipids and plasma, and reduced the mRNA levels of the fatty acid desaturases. The decreased gene expression of stearoyl-CoA desaturase suggested that the fatty acids were directed towards oxidation rather than esterification as TAG. The decreased mRNA levels of VLDL-receptor and lipoprotein lipase in the liver after SCP feeding suggested that the uptake of TAG-rich lipoprotein to the liver was decreased. To conclude, the reduced fatty liver by SCP feeding may be caused by the increased capacity for fatty acid β-oxidation in the liver, combined with changed fatty acid composition and possibly a reduced hepatic clearance of circulating VLDL. An increased awareness of the effect of dietary proteins on lipid metabolism could be of relevance in future dietary treatment of non-alcoholic fatty liver disease.

Strategies to manipulate the intestinal microbiota have been considered to promote immune health. The aim of the present study was to examine whether fructo-oligosaccharide, a typical prebiotic, could suppress antigen-specific skin inflammation by favourably changing the population of intestinal microbiota. Female BALB/c mice were fed a synthetic diet with or without fructo-oligosaccharide supplementation for 3 weeks and were then epicutaneously immunised with 2,4-dinitrofluorobenzene. Afterwards, mice continued to receive their respective diets. At 5 d after immunisation, the mice were ear challenged with the hapten. Ear swelling after the challenge was significantly reduced in the mice fed the diet supplemented with fructo-oligosaccharide than in mice fed the control diet. To characterise the change in the intestinal microbiota, DNA samples isolated from fresh faeces were subjected to PCR–denaturing gradient gel electrophoresis and real-time PCR based on 16S rDNA gene sequences. Dietary fructo-oligosaccharide altered the composition of intestinal microbiota. The numbers of bifidobacteria, but not lactobacilli, were significantly higher in mice fed the fructo-oligosaccharide-supplemented diet than in mice fed the control diet. Ear swelling was negatively correlated with the numbers of bifidobacteria in the faeces. Sequence analysis revealed that Bifidobacterium pseudolongum was the most predominant bifidobacteria in the intestine of mice fed the fructo-oligosaccharide-supplemented diet. These results suggest that consumption of fructo-oligosaccharide reduces contact hypersensitivity, which is associated with proliferation of B. pseudolongum in the intestinal tract of mice.

Dietary therapies are routinely recommended to reduce disease risk; however, there is concern they may adversely affect mood. We compared the effect on mood of a low-sodium, high-potassium diet (LNAHK) and a high-calcium diet (HC) with a moderate-sodium, high-potassium, high-calcium Dietary Approaches to Stop Hypertension (DASH)-type diet (OD). We also assessed the relationship between dietary electrolytes and cortisol, a stress hormone and marker of hypothalamic–pituitary–adrenal (HPA) axis activity. In a crossover design, subjects were randomized to two diets for 4 weeks, the OD and either LNAHK or HC, each preceded by a 2-week control diet (CD). Dietary compliance was assessed by 24 h urine collections. Mood was measured weekly by the Profile of Mood States (POMS). Saliva samples were collected to measure cortisol. The change in mood between the preceding CD and the test diet (LNAHK or HC) was compared with the change between the CD and OD. Of the thirty-eight women and fifty-six men (mean age 56·3 (sem 9·8) years) that completed the OD, forty-three completed the LNAHK and forty-eight the HC. There was a greater improvement in depression, tension, vigour and the POMS global score for the LNAHK diet compared to OD (P < 0·05). Higher cortisol levels were weakly associated with greater vigour, lower fatigue, and higher levels of urinary potassium and magnesium (r 0·1–0·2, P < 0·05 for all). In conclusion, a LNAHK diet appeared to have a positive effect on overall mood.

Saponins are naturally occurring amphiphilic molecules and have been associated with many biological activities. The aim of the present study was to investigate whether soya saponins trigger the onset of soyabean-induced enteritis in Atlantic salmon (Salmo salar L.), and to examine if dietary soya saponins increase the epithelial permeability of the distal intestine in Atlantic salmon. Seven experimental diets containing different levels of soya saponins were fed to seawater-adapted Atlantic salmon for 53 d. The diets included a fishmeal-based control diet, two fishmeal-based diets with different levels of added soya saponins, one diet containing 25 % lupin kernel meal, two diets based on 25 % lupin kernel meal with different levels of added soya saponins, and one diet containing 25 % defatted soyabean meal. The effect on intestinal morphology, intestinal epithelial permeability and faecal DM content was examined. Fish fed 25 % defatted soyabean meal displayed severe enteritis, whereas fish fed 25 % lupin kernel meal had normal intestinal morphology. The combination of soya saponins and fishmeal did not induce morphological changes but fish fed soya saponins in combination with lupin kernel meal displayed significant enteritis. Increased epithelial permeability was observed in fish fed 25 % defatted soyabean meal and in fish fed soya saponin concentrate independent of the protein source in the feed. The study demonstrates that soya saponins, in combination with one or several unidentified components present in legumes, induce an inflammatory reaction in the distal intestine of Atlantic salmon. Soya saponins increase the intestinal epithelial permeability but do not, per se, induce enteritis.

Propionibacterium freudenreichii, a food-grade bacterium able to kill colon cancer cell lines in vitro by apoptosis, may exert an anticarcinogenic effect in vivo. To assess this hypothesis, we administered daily 2 × 1010 colony-forming units (CFU) of P. freudenreichii TL133 to human microbiota-associated (HMA) rats for 18 d. Either saline or 1,2-dimethylhydrazine (DMH) was also administered on days 13 and 17 and rats were killed on day 19. The levels of apoptosis and proliferation in the mid and distal colon were assessed by terminal deoxynucleotide transferase-mediated deoxyuridine triphosphate nick end labelling (TUNEL) and proliferating cell nuclear antigen (PCNA) immunolabelling, respectively. The administration of P. freudenreichii TL133 significantly increased the number of apoptotic cells in DMH-treated rats compared to those given DMH only (P < 0·01). Furthermore, propionibacteria were able to decrease the proliferation index in the distal colon after treatment with DMH (P < 0·01). Conversely, propionibacteria alone did not exert such an effect on healthy colonic mucosa. P. freudenreichii TL133 thus facilitated the elimination of damaged cells by apoptosis in the rat colon after genotoxic insult and may play a protective role against colon cancer.

Maize with enhanced provitamin A carotenoids (biofortified), accomplished through conventional plant breeding, maintains vitamin A (VA) status in Mongolian gerbils (Meriones unguiculatus). Two studies in gerbils compared the VA value of β-cryptoxanthin with β-carotene. Study 1 (n 47) examined oil supplements and study 2 (n 46) used maize with enhanced β-cryptoxanthin and β-carotene. After 4 weeks' depletion, seven or six gerbils were killed; remaining gerbils were placed into weight-matched groups of 10. In study 1, daily supplements were cottonseed oil, and 35, 35 or 17·5 nmol VA (retinyl acetate), β-cryptoxanthin or β-carotene, respectively, for 3 weeks. In study 2, one group of gerbils was fed a 50 % biofortified maize diet which contained 2·9 nmol β-cryptoxanthin and 3·2 nmol β-carotene/g feed. Other groups were given equivalent β-carotene or VA supplements based on prior-day intake from the biofortified maize or oil only for 4 weeks. In study 1, liver retinol was higher in the VA (0·74 (sd 0·11) μmol) and β-cryptoxanthin (0·65 (sd 0·10) μmol) groups than in the β-carotene (0·49 (sd 0·13) μmol) and control (0·41 (sd 0·16) μmol) groups (P < 0·05). In study 2, the VA (1·17 (sd 0·19) μmol) and maize (0·71 (sd 0·18) μmol) groups had higher liver retinol than the control (0·42 (sd 0·16) μmol) group (P < 0·05), whereas the β-carotene (0·57 (sd 0·21) μmol) group did not. Bioconversion factors (i.e. 2·74 μg β-cryptoxanthin and 2·4 μg β-carotene equivalents in maize to 1 μg retinol) were lower than the Institute of Medicine values.

At least fourteen cohort studies have documented an inverse association between coffee consumption and risk of type 2 diabetes. We examined the prospective association between coffee and tea consumption and the risk of type 2 diabetes mellitus among British men (n 4055) and women (n 1768) from the Whitehall II cohort. During 11·7 years follow-up there were a total of 387 incident cases of diabetes confirmed by self-report of doctor's diagnosis or glucose tolerance tests. Despite an inverse association between coffee intake and 2 h post-load glucose concentration at the baseline assessment, combined caffeinated and decaffeinated coffee (hazard ratio (HR) 0·80; 95 % CI 0·54, 1·18) or only decaffeinated coffee intake (HR 0·65; 95 % CI 0·36, 1·16) was not significantly associated with diabetes risk at follow-up after adjustment for possible confounders. There was an association between tea intake and diabetes (HR 0·66; 95 % CI 0·61, 1·22; P < 0·05) after adjustment for age, gender, ethnicity and social status, which was not robust to further adjustments. There was, however, an association between combined intake of tea and coffee (two or more cups per day of both beverage) and diabetes (HR 0·68; 95 % CI 0·46, 0·99; P < 0·05) after full adjustment. In conclusion, relatively moderate intake (more than three cups per day) of coffee and tea were not prospectively associated with incidence of type 2 diabetes although there was evidence of a combined effect. The limited range of exposure and beverage consumption according to socio-economic class may explain these conflicting findings.

Fish oils (FO) – rich in EPA and DHA – may protect against colitis development. Moreover, inflammatory bowel disease patients have elevated colonic arachidonic acid (AA) proportions. So far, effects of dietary AA v. FO on colitis have never been examined. We therefore designed three isoenergetic diets, which were fed to mice for 6 weeks preceding and during 7 d dextran sodium sulfate colitis induction. The control diet was rich in oleic acid (OA). For the other two diets, 1·0 % (w/w) OA was exchanged for EPA+DHA (FO group) or AA. At 7 d after colitis induction, the AA group had gained weight (0·46 (sem 0·54) g), whereas the FO and OA groups had lost weight ( − 0·98 (sem 0·81) g and − 0·79 (sem 1·05) g, respectively; P < 0·01 v. AA). The AA group had less diarrhoea than the FO and OA groups (P < 0·05). Weight and length of the colon, histological scores and cytokine concentrations in colon homogenates showed no differences. Myeloperoxidase concentrations in plasma and polymorphonuclear cell infiltration in colon were decreased in the FO group as compared with the OA group. We conclude that in this mice model an AA-enriched diet increased colonic AA content, but did not result in more colonic inflammation as compared with FO- and OA-enriched diets. As we only examined effects after 7 d and because the time point for evaluating effects seems to be important, the present results should be regarded as preliminary. Future studies should further elucidate differential effects of fatty acids on colitis development in time.

Elderly individuals are more susceptible to gastrointestinal problems such as constipation than young adults. Furthermore, the common use of non-steroidal anti-inflammatory drugs (NSAID) among the elderly is known to further increase such gastrointestinal ailments. To describe the specific changes in elderly, intestinal microbes, their metabolites and immune markers were measured from faecal samples obtained from fifty-five elderly individuals (aged 68–88 years), using either NSAID or not, and fourteen young adults (aged 21–39 years). The faecal DM content increased with age but was significantly lower among the elderly NSAID users. The microbial metabolism was especially influenced by NSAID use and/or ageing, although fewer changes were observed in the composition of the microbial community, whilst the level of aerobes was increased in the elderly and the level of Clostridium coccoides–Eubacterium rectale reduced in the elderly NSAID users as compared with young adults. An increase in the concentrations of some branched SCFA and l-lactate but a decrease in some major SCFA concentrations were observed. Evidently, the decreased defecation frequency in the elderly directed colonic fermentation toward an unfavourable microbial metabolism but this was partially offset by the use of NSAID. Irrespective of the use of NSAID, the elderly subjects had significantly lower concentrations of faecal PGE2 than the young adults, reflecting possibly a reduced immune response. According to the present study more attention should be paid to the development of dietary products that seek to enhance bowel function, saccharolytic fermentation and immune stimulation in the elderly population.

Little is known about the effect of dietary carbohydrate, glycaemic index (GI) and glycaemic load (GL) on the risk of the metabolic syndrome, especially in populations with white rice as the staple food. The study examined the cross-sectional relationship between carbohydrate, GI, GL and risk of the metabolic syndrome. There were a total of 910 middle-aged Korean adults. Dietary carbohydrate, GI and GL were determined by an interview-administered FFQ. The metabolic syndrome was defined using the modified criteria published in the Third Report of the National Cholesterol Education Program Adult Treatment Panel III. The risk of developing the metabolic syndrome was positively related to dietary carbohydrate (P for trend = 0·03), GI (P for trend = 0·03) and GL intakes (P for trend = 0·02) in women after adjusting for potential confounding variables. Among the components of developing the metabolic syndrome, the risk of high TAG and low HDL-cholesterol were positively related to high GI and GL intakes in women. The risk of developing the metabolic syndrome was considerably higher in the highest quintiles of carbohydrate (OR 6·44; 95 % CI 2·16, 19·2), GI (OR 10·4; 95 % CI 3·24, 33·3) and GL intakes (OR 6·68; 95 % CI 2·30, 19·4) than in the lowest quintiles among women with a BMI ≥ 25 kg/m2. However, there was no difference in risk across quintiles of carbohydrate, GI and GL among women with a BMI < 25 kg/m2. In conclusion, both the quantity and quality of carbohydrate intake has a positive relationship with the risk of the metabolic syndrome in women but this relationship was dependent on the BMI level.

This study examined the effect of a pre-exercise meal with different glycaemic index (GI) and glycaemic load (GL) on immune responses to an endurance performance run. Eight men completed a preloaded 1 h run at 70 % VO2max on a level treadmill followed by a 10 km performance run on three occasions. In each trial, one of the three prescribed isoenergetic meals, i.e. high GI and high GL (H-H), high GI and low GL (H-L), or low GI and low GL (L-L) was consumed by the subjects 2 h before exercise. Carbohydrate intake (% of energy intake), GI, and GL were 65 %, 79·5, and 82·4 for H-H; 36 %, 78·5, and 44·1 for H-L; 65 %, 40·2, and 42·1 for L-L, respectively. The running time for the three trials was approximately 112 min at 70 % VO2max for the first hour and 76 % VO2max for the last 52 min. Consumption of pre-exercise high-carbohydrate meals (H-H and L-L) resulted in less perturbation of the circulating numbers of leucocytes, neutrophils and T lymphocyte subsets, and in decreased elevation of the plasma IL-6 concentrations immediately after exercise and during the 2 h recovery period compared with the H-L trial. These responses were accompanied by an attenuated increase in plasma IL-10 concentrations at the the end of the 2 h recovery period. The amount of carbohydrate consumed in the pre-exercise meal may be the most important influencing factor rather than the type of carbohydrate in modifying the immunoendocrine response to prolonged exercise.

Very long-chain n-3 PUFA from fish are suggested to play a role in the development of the brain. Fish oil feeding results in higher proportions of n-3 PUFA in the brains of newborn piglets. However, the effect of fish oil on the fatty acid composition of specific cerebral brain lobes in juvenile pigs is largely uninvestigated. This study examined the effect of a fish oil diet on the fatty acid composition of the frontal, parietal, temporal and occipital brain lobes in juvenile pigs (7 weeks old). Pigs were randomly allocated to a semipurified pig diet containing either 4 % (w/w) fish oil (n 19) or 4 % (w/w) high-oleic acid sunflower oil (HOSF diet, n 18) for a period of 8 weeks. The fish oil diet resulted in significantly higher proportions (%) of DHA in the frontal (10·6 (sd1·2)), parietal (10·2 (sd1·5)) and occipital brain lobes (9·9 (sd 1·3)), but not in the temporal lobe (7·7 (sd1·6)), compared with pigs fed the HOSF diet (frontal lobe, 7·5 (sd1·0); parietal lobe, 8·1 (sd 1·3); occipital lobe, 7·3 (sd1·2), temporal lobe, 6·6 (sd1·2). Moreover, the proportion of DHA was significantly lower in the temporal lobe compared with the frontal, parietal and occipital brain lobes in pigs fed a fish oil diet. In conclusion, the brains of juvenile pigs appear to be responsive to dietary fish oil, although the temporal brain lobe is less responsive compared with the other three brain lobes. The functional consequences of these differences are a challenging focus for future investigation.

Concerns about risks for older people with vitamin B12 deficiency have delayed the introduction of mandatory folic acid fortification in the UK. We examined the risks of anaemia and cognitive impairment in older people with low B12 and high folate status in the setting of voluntary fortification in the UK. Data were obtained from two cross-sectional studies (n 2403) conducted in Oxford city and Banbury in 1995 and 2003, respectively. Associations (OR and 95 % CI) of cognitive impairment and of anaemia with low B12 status (holotranscobalamin < 45 pmol/l) with or without high folate status (defined either as serum folate >30 nmol/l or >60 nmol/l) were estimated after adjustment for age, sex, smoking and study. Mean serum folate levels increased from 15·8 (sd 14·7) nmol/l in 1995 to 31·1 (sd 26·2) nmol/l in 2003. Serum folate levels were greater than 30 nmol/l in 9 % and greater than 60 nmol/l in 5 %. The association of cognitive impairment with low B12 status was unaffected by high v. low folate status (>30 nmol/l) (OR 1·50 (95 % CI 0·91, 2·46) v. 1·45 (95 % CI 1·19, 1·76)), respectively. The associations of cognitive impairment with low B12 status were also similar using the higher cut-off point of 60 nmol/l for folate status ((OR 2·46; 95 % CI 0·90, 6·71) v. (1·56; 95 % CI 1·30, 1·88)). There was no evidence of modification by high folate status of the associations of low B12 with anaemia or cognitive impairment in the setting of voluntary fortification, but periodic surveys are needed to monitor fortification.

In mammals, (n-3) PUFA and conjugated linoleic acids (CLA) act as activators of PPARα and alter nuclear concentrations of sterol regulatory element-binding proteins (SREBP) in the liver, and thereby influence hepatic lipid catabolism and synthesis. In this study, we investigated the hypothesis that (n-3) PUFA and CLA exert similar effects in the liver of laying hens. Thirty hens (64 weeks old) were fed diets containing 30 g/kg of sunflower oil (control), fish oil (salmon oil) or CLA in TAG form (containing predominantly cis-9, trans-11 CLA and trans-10, cis-12 CLA) for 5 weeks. Hens fed fish oil had a higher expression of some PPARα target genes and a lower nuclear concentration of SREBP-2 in the liver and lower concentrations of cholesterol and TAG in plasma than control hens. Nuclear concentration of SREBP-1 and its target genes involved in lipogenesis were not altered in hens fed fish oil. Hens fed CLA had increased concentrations of TAG and cholesterol in the liver. However, their mRNA levels of PPARα target genes and nuclear concentrations of SREBP-1 and SREBP-2 as well as mRNA levels of their target genes in the liver were largely unchanged compared to control hens. The results of this study suggest that (n-3) PUFA cause a moderate activation of PPARα and lower cholesterol synthesis but do not impair fatty acid synthesis in the liver of laying hens. CLA lead to an accumulation of TAG and cholesterol in the liver of hens by mechanisms to be elucidated in further studies.

Oxidative modification of LDL is thought to play an important role in the development of atherosclerosis. Susceptibility of LDL to peroxidation may partly depend on the compositional characteristics of the antioxidant and fatty acid content. The aim of this study was to examine the association between levels of antibodies to oxidized LDL and the various serum fatty acids in women. A total of 465 women aged 18–65 years were selected randomly from the adult population census of Pizarra, a town in southern Spain. Measurement of anti-oxidized-LDL was done by ELISA and the fatty acid composition of serum phospholipids was determined by GC. The levels of anti-oxidized-LDL antibodies were significantly related with age (r − 0·341, P < 0·001), BMI (r − 0·239, P < 0·001), waist:hip ratio (r − 0·285, P < 0·001), glucose (r − 0·208, P < 0·001), cholesterol (r − 0·243, P < 0·001), LDL-cholesterol (r − 0·185, P = 0·002), EPA (r − 0·159, P = 0·003), DHA (r − 0·121, P = 0·026), and the sum of the serum phospholipid n-3 PUFA (r − 0·141, P = 0·009). Multiple regression analysis showed that the variables that explained the behaviour of the levels of anti-oxidized-LDL antibodies were age (P < 0·001) and the serum phospholipid EPA (P < 0·001). This study showed that the fatty acid composition of serum phospholipids, and especially the percentage of EPA, was inversely related with the levels of anti-oxidized-LDL antibodies.