Lipase-catalyzed incorporation of n−3 PUFA into palm oil

Two immobilized lipases, IM60 from Rhizomucor miehei and QLM from Alcaligenes sp., were used as biocatalysts for the modification of the FA composition of palm oil by incorporating n−3 PUFA. Acidolysis and interesterification reactions were conducted with hexane as organic solvent, and the products were analyzed by using GLC. After a 24-h incubation in hexane, there was an average incorporation of 20.8% EPA and 15.6% DHA into palm oil, respectively, while the percentages of palmitic and oleic acids in palm oil decreased by 28.8 and 11.8%, respectively. Higher EPA and DHA incorporation was obtained when EPAX (fish oil concentrate high in n−3 PUFA) was used in the ethyl ester form (interesterification reaction) than in the free acid form (acidolysis) in the presence of Lipozyme (IM60 lipase. Lipase QLM was found to discriminate against EPA, and it showed slightly better catalytic activity for DHA in the free acid form than in the ethyl ester form. Generally, as the mole ratio of the acyl donor to TAG increased, the percentage incorporation of EPA and DHA increased; however, reactions catalyzed by Lipozyme IM60 did not show increases in the incorporation beyond a TAG/EPAX mole ratio of 3. When limitations due to mass transfer were not a factor, an increase in the reactant amount also gave an increase in the percentage incorporation of the n−3 PUFA. Palm oil containing EPA and DHA was successfully produced and may be beneficial in certain food and nutritional applications.     

Effect of n−3 polyunsaturated fatty acid supplementation on lipid peroxidation of rat organs

The present study was undertaken in order to reexamine the effect of n−3 polyunsaturated fatty acid (PUFA)-rich diet supplementation on lipid peroxidation and vitamin E status of rat organs. Male Wistar rats were fed a diet containing safflower or fish oil at 50 g/kg diet and an equal amount of vitamin E at 59 mg/kg diet (1.18 g/kg oil; and 1.5 g/kg PUFA in safflower oil diet, and 4.3 g/kg PUFA in fish oil diet) for 6 wk. Fatty acid composition of total lipids of brain, liver, heart, and lung of rats fed fish oil was rich in n−3 PUFA, whereas that of each organ of rats fed safflower oil was rich in n−6 PUFA. The vitamin E levels in liver, stomach, and testis of the fish oil diet group were slightly lower than those of the safflower oil diet group, but the levels in brain, heart, lung, kidney, and spleen were not different between the two diet groups. The levels of phospholipid hydroperoxides were determined by the high-performance liquid chromatography-chemiluminescence method and the levels of thiobarbituric acid-reactive substances (TBARS) were determined at pH 3.5 in the presence of butylated hydroxytoluene with or without EDTA. Levels of phospholipid hydroperoxides and TBARS in the brain, liver, heart, lung, kidney, spleen, stomach and testis of the fish oil diet group were similar to those of the safflower oil diet group. The results indicate that high fish oil intake does not induce increased levels of phospholipid hydroperoxides and TBARS in rat organs.     

Enhanced incorporation of n−3 fatty acids from fish compared with fish oils

This work was undertaken to study the impact of the source of n−3 FA on their incorporation in serum, on blood lipid composition, and on cellular activation. A clinical trial comprising 71 volunteers, divided into five groups, was performed. Three groups were given 400 g smoked salmon (n=14), cooked salmon (n=15), or cooked cod (n=13) per week for 8 wk. A fourth group was given 15 mL/d of cod liver oil (CLO) (n=15), and a fifth group served as control (n=14) without supplementation. The serum content of EPA and DHA before and after intervention revealed a higher rise in EPA and DHA in the cooked salmon group (129% rise in EPA and 45% rise in DHA) as compared with CLO (106 and 25%, respectively) despite an intake of EPA and DHA in the CLO group of 3.0 g/d compared with 1.2 g/d in the cooked salmon group. No significant changes were observed in blood lipids, fibrinogen, fibrinolysis, or lipopolysaccharide (LPS)-induced tissue factor (TF) activity, tumor necrosis factor-α (TNFα), interleukin-8 (IL-8), leukotriene B₄ (LTB₄), and thromboxane B₂ (TxB₂) in whole blood. EPA and DHA were negatively correlated with LPS-induced TNFα, IL-8, LTB₄, TxB₂, and TF in whole blood. In conclusion, fish consumption is more effective in increasing serum EPA and DHA than supplementing the diet with fish oil. Since the n−3 FA are predominantly in TAG in fish as well as CLO, it is suggested that the larger uptake from fish than CLO is due to differences in physiochemical structure of the lipids.     

Maternal fish oil supplementation in lactation: Effect on visual acuity and n−3 fatty acid content of infant erythrocytes

Studies on formula-fed infants indicate a beneficial effect of dietary DHA on visual acuity. Cross-sectional studies have shown an association between breast-milk DHA levels and visual acuity in breast-fed infants. The objective in this study was to evaluate the biochemical and functional effects of fish oil (FO) supplements in lactating mothers. In this double-blinded randomized trial, Danish mothers with habitual fish intake below the 50th percentile of the Danish National Birth Cohort were randomized to microencapsulated FO [1.3 g/d long-chain n−3 FA (n−3 LCPUFA)] or olive oil (OO). The intervention started within a week after delivery and lasted 4 mon. Mothers with habitual high fish intake and their infants were included as a reference group. Ninety-seven infants completed the trial (44 OO-group, 53 FO-group) and 47 reference infants were followed up. The primary outcome measures were: DHA content of milk samples (0, 2, and 4 mon postnatal) and of infant red blood cell (RBC) membranes (4 mon postnatal), and infant visual acuity (measured by swept visual evoked potential at 2 and 4 mon of age). FO supplementation gave rise to a threefold increase in the DHA content of the 4-mon milk samples (P<0.001). DHA in infant RBC reflected milk contents (r=0.564, P<0.001) and was increased by almost 50% (P<0.001). Infant visual acuity was not significantly different in the randomized groups but was positively associated at 4 mon with infant RBC-DHA (P=0.004, multiple regression). We concluded that maternal FO supplementation during lactation did not enhance visual acuity of the infants who completed the intervention. However, the results showed that infants with higher RBC levels of n−3 LCPUFA had a better visual acuity at 4 mon of age, suggesting that n−3 LCPUFA may influence visual maturation.     

A randomized controlled trial of the effect of fish oil supplementation in late pregnancy and early lactation on the n−3 fatty acid content in human breast milk

The aim of this research was to investigate the effect of fish oil supplementation, in the third trimester of pregnancy and early lactation period of healthy pregnant Danish women. Forty-four pregnant women were randomly allocated to fish oil supplementation (1.3 g EPA and 0.9 g DHA per day) from week 30 of gestation (FO-group) or to a control regimen (olive oil or no oil; controls). The FO-group was randomly subdivided into women stopping fish oil supplementation at delivery [FO(pregn)], and women continuing supplementation for an, additional 30 d [FO(pregn/lact)]. Thirty-six women agreed to collect milk samples at days 4, 16, and 30 postpartum. The FA composition of the milk samples was determined by GLC. At days 4, 16, and 30 in lactation, FO(pregn/lact) women (n=12) had, respectively 2.3 (P=0.001), 4.1 (P=0.001), and 3.3 (P=0.001) times higher mean contents of LCPUFA(n−3) in their breast milk compared with controls (n=13), and 1.7 (P=0.005), 2.8 (P=0.001), and 2.8 (P=0.001), times higher LCPUFA(n−3) contents, respectively, at these days compared with FO(pregn) women (n=11). The latter group did not differ significantly from controls with regard to LCPUFA(n−3) content in the breast milk. Similar results were obtained when analyzing separately for effects on the milk content of DHA. Dietary supplementation with 2.7 g LCPUFA(n−3) per day from week 30 of gestation and onward more than tripled the LCPUFA(n−3) content in early breast milk; supplementation limited to pregnancy only was much less effective.     

n−3 and n−6 fatty acid enrichment by dietary fish oil and phospholipid sources in brain cortical areas and nonneural tissues of formula-fed piglets

Sufficient availability of both n-3 and n-6 long-chain polyunsaturated fatty acids (LCPUFA) is required for optimal structural and functional development in infancy. The question has been raised as to whether infant formulae would benefit from enrichment with 20 and 22 carbon fatty acids. To address this issue, we determined the effect of fish oil and phospholipid (LCPUFA) sources on the fatty acid composition of brain cortical areas and nonneural tissues of newborn piglets fed artificially for 2 wk. They were fed sow milk, a control formula, or the formula enriched with n-3 fatty acids from a low-20:5n-3 fish oil added at a high or a low concentration, or the formula enriched with n-3 and n-6 fatty acids from either egg yolk- or pig brain-phospholipids. Both the fish oil- and the phospholipid-enriched formula produced significantly higher plasma phospholipid 22:6n-3 concentrations than did the control formula. The 22:6n-3 levels in the brain, hepatic, and intestinal phospholipids were significantly correlated with plasma values, whereas cardiac 22:6n-3 content appeared to follow a saturable dose-response. Feeding sow milk resulted in a much higher 20:4n-6 content in nonneural tissues than did feeding formula. Supplementation with egg phospholipid increased the 20:4n-6 content in the heart, red blood cells, plasma, and intestine in comparison to the control formula, while pig brain phospholipids exerted this effect in the heart only. The addition of 4.5% fish oil in the formula was associated with a decline in 20:4n-6 in the cortex, cerebellum, heart, liver, and plasma phospholipids, whereas using this source at 1.5% limited the decline to the cerebellum, liver, and plasma. Whatever the dietary treatment, the phosphatidylethanolamine 20:4n-6 level was 10–20% higher in the brain temporal lobe than in the parietal, frontal, and occipital lobes in the temporal lobe by administering the formula enriched with egg or brain phospholipids. In conclusion, feeding egg phospholipids to neonatal pigs increased both the 22:6n-3 content in the brain and the 20:4n-6 content in the temporal lobe cortex. This source also increased the 22:6n-3 levels in nonneural tissues with only minor alterations of 20:4n-6. These data support the notion that infant formulae should be supplemented with both 22:6n-3 and 20:4n-6 rather than with 22:6n-3 alone.     

Cigarette smoke negatively and dose-dependently affects the biosynthetic pathway of the n−3 polyunsaturated fatty acid series in human mammary epithelial cells

Maternal smoking during pregnancy has been associated with a reduced content of n−3 long-chain PUFA (LC-PUFA) in breast milk, thereby reducing the intake of key nutrients by the infants. We postulated that the mammary gland is affected by maternal smoking in the process of n−3 LC-PUFA secretion into milk. This prompted us to investigate the effects of cigarette smoke on the synthesis of n−3 LC-PUFA in vitro by using a line of healthy epithelial cells from the human mammary gland, MCF-10A. Cells were exposed to cigarette smoke under controlled conditions by adding to the medium aliquots of horse serum containing smoke components, as analyzed by GC-MS. The major findings concern the inhibition of both the conversion of the precursor ¹⁴C-ALA (α-linolenic acid) to n−3 LC-PUFA and of the Δ5 desaturation step (assessed by HPLC analysis with radiodetection of n−3 FAME) following exposure to minimal doses of smoke-enriched serum, and the dose-dependent relationship of these effects. The data indicate that exposure to cigarette smoke negatively affects the synthesis of n−3 LC-PUFA from the precursor in mammary gland cells.     

Effect of n−3 fatty acid supplementation on lipid peroxidation and protein aggregation in rat erythrocyte membranes

Human erythrocytes in the circulation undergo dynamic oxidative damage involving membrane lipid peroxidation and protein aggregation during aging. The present study was undertaken to determine the effect of n−3 fatty acid supplementation on lipid peroxidation and protein aggregation in the circulation and also the in vitro susceptibility of rat erythrocyte membranes to oxidative damage. Wistar male rats were fed a diet containing n−6 fatty acid-rich safflower oil or n−3 fatty acid-rich fish oil with an equal amount of vitamin E for 6 wk. n−3 Fatty acid content in erythrocyte membranes of rats fed fish oil was significantly higher than that of rats fed safflower oil. The degree of membrane lipid peroxidation and protein aggregation of rats fed fish oil was not significantly higher than that of rats fed safflower oil when the amounts of phospholipid hydroper-oxides, thiobarbituric acid-reactive substances, and detergent-insoluble protein aggregates were measured. When isolated erythrocytes were oxidized under aerobic conditions in the presence of Fe(III), the degree of membrane lipid peroxidation of erythrocytes from rats fed fish oil was increased to a greater extent than that of rats fed safflower oil, whereas the degree of membrane protein aggregation of both groups was increased in a similar extent. Hence, n−3 fatty acid supplementation did not affect lipid peroxidation and protein aggregation in membranes of circulating rat erythrocytes, and the supplementation increased the susceptibility of isolated erythrocytes to lipid peroxidation, but not to protein aggregation, under the aerobic conditions. If a sufficient amount of vitamin E is supplied, n−3 fatty acid supplementation may give no undesirable oxidative effects on rat erythrocytes in the circulation.     

Effect of dietary n−6 and n−3 polyunsaturated fatty acids on peroxidizability of lipoproteins in steers

The susceptibility of major plasma lipoproteins to lipoperoxidation was studied in relation to the FA composition of their neutral and polar lipids in steers given PUFA-rich diets. Two trials used, respectively, 18 (“sunflower” experiment, S) or 24 (“linseed” experiment, L) crossbred Salers x Charolais steers. Each involved three dietary treatments over a 70-d period: a control diet (CS or CL diets) consisting of hay and concentrate, or the same diet supplemented with oilseeds (4% diet dry matter) fed either as seeds (SS or LS diets) or continuously infused into the duodenum (ISO or ILO diets). Compared with control diets, ISO and ILO treatments tended to decrease the resistance time of LDL and HDL classes to peroxidation, mainly owing to the enrichment of their polar and neutral lipids with PUFA. With diets SS and LS, sensitivity of major lipoprotein classes (LDL, light and heavy HDL) was not affected because ruminal hydrogenation of dietary PUFA decreased their incorporation into lipoparticles. ISO and ILO treatments induced a more important production of conjugated dienes and hydroperoxides generated by peroxidation in the three lipoprotein classes due to the higher amounts of PUFA esterified in lipids of the core and the hydrophilic envelope of particles. The production of malondialdehyde (MDA) increased in steers fed linseed supplements, indicating that MDA production did not occur with linoleic acid provided by sunflower oil supplements. Thus, plasma peroxidation of PUFA generates toxic products in steers fed diets supplemented with PUFA and can be deleterious for the health of the animal during long-term treatment.     

Effects of dietary n−3 polyunsaturated fatty acids on T-Cell membrane composition and function

Dietary n−3 PUFA have been shown to attenuate T-cell-mediated inflammation, in part, by suppressing T-cell activation and proliferation. n−3 PUFA have also been shown to promote apoptosis, another important mechanism for the prevention of chronic inflammation by maintaining T-cell homeostasis through the contraction of populations of activated T cells. Recent studies have specifically examined Fas death receptor-mediated activation-induced cell death (AICD), since it is the form of apoptosis associated with peripheral T-cell deletion involved in immunological tolerance and T-cell homeostasis. Data from our laboratory indicate that n−3 PUFA promote AICD in T helper 1 polarized cells, which are the mediators of chronic inflammation. Since Fas and components of the deathinducing signaling complex are recruited to plasma membrane microdomains (rafts), the effect of dietary n−3 PUFA on raft composition and resident protein localization has been the focus of recent investigations. Indeed, there is now compelling evidence that dietary n−3 PUFA are capable of modifying the composition of T-cell membrane microdomains (rafts). Because the lipids found in membrane microdomains actively participate in signal transduction pathways, these results support the hypothesis that dietary n−3 PUFA influence signaling complexes and modulate T-cell cytokinetics in vivo by altering T-cell raft composition.     

Metabolism of n−3 and n−6 fatty acids in Atlantic salmon liver: Stimulation by essential fatty acid deficiency

Oxidation, esterification, desaturation, and elongation of [1-¹⁴C]18∶2n−6 and [1-¹⁴C]18∶3n−3 were studied using hepatocytes from Atlantic salmon (Salmo salar I.) maintained on diets deficient in n−3 and n−6 polyunsaturated fatty acids (PUFA) or supplemented with n−3 PUFA. For both dietary groups, radioactivity from 18∶3n−3 was incoporated into lipid fractions two to three times faster than from 18∶2n−6, and essential fatty acids (FFA) deficiency doubled the incorporation. Oxidation to CO₂ was very low and was independent of substrate or diet, whereas oxidation to acid-soluble products was stimulated by EFA deficiency. Products from 18∶2n−6 were mainly 18∶3n−6, 20∶3n−6, and 20∶4n−6, with minor amounts of 20∶2n−6 and 22∶5n−6. Products from 18∶3n−3 were mainly 18∶4n−3, 20∶5n−3, and 22∶6n−3, with small amounts of 20∶3n−3. The percentage of 22∶6n−3 in the polar lipid fraction of EFA-deficient hepatocytes was fourfold higher than in n−3 PUFA-supplemented cells. This correlated well with our other results obtained after abdominal injection of [1-¹⁴C]18∶3n−3 and [1-¹⁴C]18∶2n−6. In hepatocytes incubated with [4,5-³H]-22∶6n−3, 20∶5n−3 was the main product. This retrocon-version was increased by EFA deficiency, as was peroxisomal β-oxidation activity. This study shows that 18∶2n−6 and 18∶3n−3 can be elongated and desaturated in Atlantic salmon liver, and that this conversion and the activity of retroconversion of very long chain PUFA is markedly enhanced by FFA deficiency.     

Effects of dietary supplementation of saturated fatty acids and of n−6 or n−3 polyunsaturated fatty acids on plasma and red blood cell membrane phospholipids and deformability in weanling guinea pigs

The fatty acid composition of plasma cholesteryl esters, plasma phospholipids, red blood cell (RBC) membrane phosphatidylcholine (corresponding to the outer membrane leaflet), and phosphatidylethanolamine (corresponding to the inner membrane leaflet) was investigated in weanling guinea pigs fed with diets of cacao (saturated fatty acids), sunflower oil [n−6 polyunsaturated fatty acids (PUFA)] or fish oil (n−3 PUFA) for 20 wk. RBC deformation was measured by means of a cell-transit analyzer (filtration) and a cone-plate rheoscope. The contents of saturated fatty acids in plasma phospholipids and RBC membrane leaflets were similar in all three groups. Diets with sunflower oil resulted in a high content of linoleic acid in plasma cholesteryl esters and in the outer leaflet of RBC membranes. Fatty acids of fish oil were mainly incorporated in plasma phospholipids and in the inner leaflet of RBC membranes. The arachidonic acid content was high in all groups in the plasma phospholipids and in the inner leaflet. The n−6 and n−3 PUFA were mainly incorporated in the inner leaflet. In all groups the polyunsaturated/saturated fatty acid ratio and the total PUFA content were similar in the inner RBC membrane. The RBC filtration times and the RBC deformation indices were not affected by the dietary treatment.     

Dietary modulation of fatty acid profiles and oxidative status of rat hepatocyte nodules: Effect of different n−6/n−3 fatty acid ratios

Male Fischer rats were fed the AIN76A diet containing varying n−6/n−3 FA ratios using sunflower oil (SFO), soybean oil (SOY), and SFO supplemented with EPA-50 and GLA-80 (GLA) as fat sources. Hepatocyte nodules, induced using diethylnitrosamine followed by 2-acetylaminofluorene/partial hepatoctomy promotion, were harvested, with surrounding and respective dietary control tissues, 3 mon after partial hepatectomy. The altered growth pattern of hepatocyte nodules in rats fed SFO is associated with a distinct lipid pattern entailing an increased concentration of PE, resulting in increased levels of 20∶4n−6. In addition, there is an accumulation of 18∶1n−9 and 18∶2n−6 and a decrease in the end products of the n−3 metabolic pathway in PC, suggesting a dysfunctional Δ-6-desaturase enzyme. The hepatocyte nodules of the SFO-fed rats exhibited a significantly reduced lipid peroxidation level that was associated with an increaser in the glutathione (GSH) concentration. The low n−6/n−3 FA ratio diets significantly decreased 20∶4n−6 in PC and PE phospholipid fractions with a concomitant increase in 20∶5n−3, 22∶5n−3, and 22∶6n−3. The resultant changes in the 20∶4/20∶5 FA ratio and the 20∶3n−6 FA level in the case of the GLA diet suggest a reduction of prostaglandin synthesis of the 2-series. The GLA diet also counteracted the increased level of 20∶4n−6 in PE by equalizing the nodule/surrounding ratio. The low n−6/n−3 ratio diets significantly increased lipid peroxidation levels in hepatocyte nodules, mimicking the level in the surrounding and control tissue while GSH was decreased. An increase in n−3 FA levels and oxidative status resulted in a reduction in the number of glutathione-S-transferase positive foci in the liver of the GLA-fed rats. Modulation of cancer development with low n−6/n−3 ratio diets containing specific dietary FA could be a promising tool in cancer intervention in the liver.     

Effect of n−3 fatty acid deficiency on fatty acid composition and metabolism of aminophospholipids in rat brain synaptosomes

Docosahexaenoic acid (DHA, 22∶6n−3) is one of the major polyunsaturated fatty acids esterified predominantly in aminophospholipids such as ethanolamine glycerophospholipid (EtnGpl) and serine glycerophospholipid (SerGpl) in the brain. Synaptosomes prepared from rats fed an n−3 fatty acid-deficient safflower oil (Saf) diet had significantly decreased 22∶6n−3 content with a compensatory increased 22∶5n−6 content when compared with rats fed an n−3 fatty acid-sufficient perilla oil (Per) diet. When the Saf group was shifted to a diet supplemented with safflower oil plus 22∶6n−3 (Saf+DHA) after weaning, 22∶6n−3 content was found to be restored to the level of the Per group. The uptake of [³H]ethanolamine and its conversion to [³H]EtnGpl did not differ significantly among the three dietary groups, whereas the formation of [³H]lysoEtnGpl from [³H]ethanolamine was significantly lower in the Saf group than in the other groups. The uptake of [³H]serine, its incorporation into [³H]SerGpl, and the conversion into [³H]EtnGpl by decarboxylation of [³H]SerGpl did not differ among the three dietary groups. The observed decrease in lysoEtnGpl formation associated with a reduction of 22∶6n−3 content in rat brain synaptosomes by n−3 fatty acid deprivation may provide a clue to reveal biochemical bases for the dietary fatty acids-behavior link.     

Dietary n−3 polyunsaturated fatty acids increase T-lymphocyte phospholipid mass and acyl-CoA binding protein expression

Dietary flaxseed oil, which is enriched in α-linolenic acid, and fish oil, which is enriched inEPA and DHA, possess anti-inflammatory properties when compared with safflower oil, which is enriched in linoleic acid. The influence of flaxseed oil and fish oil feeding on lipid metabolism in T-lymphocytes is currently unknown. This study directly compared the effects of feeding safflower oil, flaxseed oil, and fish oil for 8 wk on splenic T-lymphocyte proliferation, phospholipid mass, and acyl-CoA binding protein expression in the rat. The data show that both flaxseed oil and fish oil increased acyl-CoA binding protein expression and phosphatidic acid mass in unstimulated T-lymphocytes when compared with safflower oil feeding. Fish oil feeding increased cardiolipin mass, whereas flaxseed oil had no effect. After stimulation, flaxseed oil and fish oil blunted T-lymphocyte interleukin-2 production and subsequent proliferation, which was associated with the lack of incraased acyl-CoA binding protein expression. The results reported show evidence for a novel mechanism by which dietary flaxseed oil and fish oil suppress T-lymphocyte proliferation via changes in acyl-CoA binding protein expression and phospholipid mass.     

A biomarker of n−3 compliance in patients taking fish oil for rheumatoid arthritis

Dietary fish oil supplements have been shown to have benefits in rheumatoid arthritis (RA), other inflammatory diseases, and in cardiovascular disease. As with any medical advice, variability will exist with regard to adherence and consequent biochemical or pharmacophysiologic effects. The aim was to explore the utility of plasma phospholipid EPA as a measure of n−3 PUFA intake and response to standardized therapeutic advice given in an outpatient or office practice setting, to increase dietary n−3 PUFA, including a fish oil supplement. Patients with early RA were given verbal and written advice to alter their dietary n−3 PUFA intake, including ingestion of 20 mL of bottled fish oil on juice daily. The advice included instructions to increase n−3 PUFA and to avoid foods rich in n−6 PUFA. Every 3 mon, blood samples were obtained for analysis of plasma phospholipid FA. Plasma phospholipid EPA was used as the primary index of n−3 PUFA intake. A diverse response was seen, with about one-third of patients achieving a substantial elevation of plasma phospholipid EPA over the 12-mon study period. A third had little change, with the remainder achieving intermediate levels. Data obtained longitudinally from individual patients indicated that substantial elevations of EPA (>5% total plasma phospholipid FA) could be maintained for more than 3 yr. Plasma phospholipid EPA is a convenient measure of adherence to advice to take a dietary n−3 PUFA-rich fish oil supplement. This measure may prove a useful adjunct to intention to treat analyses in determining the effect of dietary fish oil supplements on long-term outcomes in arthritis and other chronic inflammatory diseases. It may also provide a guide to the effectiveness of therapeutic and preventive messages designed to increase n−3 PUFA intake.     

n−3 fatty acid enrichment of edible tissue of poultry: A review

There is clear evidence of the nutritional benefits of consuming long-chain n−3 PUFA, which are found predominantly in oily fish. However, oily fish consumption, particularly in the United Kingdom, is declining, as is the consumption of all meats with the exception of poultry, which has increased in consumption by 73% in the last 30 yr. This pattern, if less marked, is reflected throughout Europe, and therefore one means of increasing long-chain n−3 PUFA consumption would be to increase the long-chain n−3 PUFA content in the edible tissues of poultry. This review considers the feasibility of doing this, concentrating particularly on chickens and turkeys. It begins by summarizing the benefits to human health of consuming greater quantities of n−3 FA and the sources of n−3 PUFA in the human diet. The literature on altering the FA composition of poultry meat is then reviewed, and the factors affecting the incorporation of n−3 PUFA into edible tissues of poultry are investigated. The concentration of α-linolenic acid (ALA) in the edible tissues of poultry is readily increased by increasing the concentration of ALA in the birds' diet (particularly meat with skin, and dark meat to a greater extent than white meat). The concentration of EPA in both white and dark meat is also increased when the birds' diet is supplemented with EPA, although supplementing the diet with the precursor (ALA) does not result in a noticeable increase in EPA content in the edible tissues. Although supplementing the birds' diets with relatively high concentrations of DHA does result in an increased concentration of DHA in the tissues, the relationship between dietary and tissue concentrations of DHA is much weaker than that observed with ALA and EPA. The impact that altering the FA composition of edible poultry tissue may have on the organoleptic and storage qualities of poultry products is also considered.     

n−3 fatty acids and human health: Defining strategies for public policy

The last quarter of the 20th century was characterized by an increase in the consumer's interest in the nutritional aspects of health. As a result, governments began to develop dietary guidelines in addition to the traditional recommended dietary allowances, which have been superseded now by dietary reference intakes. In addition to governments, various scientific societies and nongovernmental organizations have issued their dietary advice to combat chronic diseases and obesity. Human beings evolved on a diet that was balanced in n?6 and n?3 essential fatty acid intake, whereas Western diets have a ratio of n?6/n?3 of 16.74. The scientific evidence is strong for decreasing the n?6 and increasing the n?3 intake to improve health throughout the life cycle. This paper discusses the reasons for this change and recommends the establishment of a nutrition and Food Policy, instead of a Food and Nutrition Policy, because the latter subordinates the nutritional aspects to the food policy aspects. Nutrition and food planning comprise a tool of nutrition and food policy, whose objectives are the achievement of the adequate nutrition of the population as defined by nutritional science. The scientific basis for the development of a public policy to develop dietary recommendations for essential fatty acids, including a balanced n?6/n?3 ratio is robust. What is needed is a scientific consensus, education of professionals and the public, the establishment of an agency on nutrition and food policy at the national level, and willingness of governments to institute changes. Education of the public is essential to demand changes in the food supply     

Influence of dietary supplementation with long-chain n−3 or n−6 polyunsaturated fatty acids on blood inflammatory cell populations and functions and on plasma soluble adhesion molecules in healthy adults

Greatly increasing the amounts of flaxseed oil [rich in α-linolenic acid (ALNA)] or fish oil (FO); [rich in eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)] in the diet can decrease inflammatory cell functions and so might impair host defense. The objective of this study was to determine the effect of dietary supplementation with moderate levels of ALNA, γ-linolenic acid (GLA), arachidonic acid (ARA), DHA, or FO on inflammatory cell numbers and functions and on circulating levels of soluble adhesion molecules. Healthy subjects aged 55 to 75 yr consumed nine capsules per day for 12 wk. The capsules contained placebo oil (an 80∶20 mix of palm and sunflowerseed oils) or blends of placebo oil with oils rich in ALNA, GLA, ARA, or DHA or FO. Subjects in these groups consumed 2 g ALNA; approximately 700 mg GLA, ARA, or DHA; or 1 g EPA plus DHA (720 mg EPA+280 mg DHA) daily from the capsules. Total fat intake from the capsules was 4 g per day. None of the treatments affected inflammatory cell numbers in the bloodstream; neutrophil and monocyte phagocytosis or respiratory burst in response to E. coli; production of tumor necrosis factor-α, interleukin-1β, and interleukin-6 in response to bacterial lipopolysaccharide; or plasma concentrations of soluble intercellular adhesion molecule-1. In contrast, the ALNA and FO treatments decreased the plasma concentrations of soluble vascular cell adhesion molecule-1 (16 and 28% decrease, respectively) and soluble E-selectin (23 and 17% decrease, respectively). It is concluded that, in contrast to previous reports using higher amounts of these fatty acids, a moderate increase in consumption of long-chain n−6 or n−3 polyunsaturated fatty acids does not significantly affect inflammatory cell numbers or neutrophil and monocyte responses in humans and so would not be expected to cause immune impairment. Furthermore, we conclude that moderate levels of ALNA and FO, which could be incorporated into the diet, can decrease some markers of endothelial activation and that this mechanism of action may contribute to the reported health benefits of n−3 fatty acids.