The effect of dietary trans α-linolenic acid on plasma lipids and platelet fatty acid composition: the TransLinE study (original) (raw)
Related papers
British Journal of Nutrition, 2001
Trans isomers of a-linolenic acid, which are formed by deodorization of refined vegetable oils, can be found in significant amounts in edible oils. Effects of trans a-linolenic acid on plasma lipoproteins are unknown. We therefore investigated the effects of trans a-linolenic acid on plasma lipids and lipoproteins in healthy European men. Eighty-eight healthy men from three European countries (France, Scotland, UK and the Netherlands) first consumed for 6 weeks a diet with experimental oils`free' of trans fatty acids (run-in period). For the next 6 weeks, they were randomly allocated to a diet with experimental oils`high' or`low' in trans a-linolenic acid. Daily total trans a-linolenic acid intake in the high trans group was 1410 (range 583± 2642) mg. Experimental oils were provided as such, or incorporated into margarines, cheeses, muffins and biscuits. The high trans a-linolenic acid diet significantly increased the plasma LDL-:HDL-cholesterol ratio by 8´1 % (95 % CI 1´4, 15´3; P 0´02Y and the total cholesterol:HDL-cholesterol ratio by 5´1 % (95 % CI 0´4, 9´9; P 0´03 compared with the low-trans diet. This was largely explained by an increase in LDL-cholesterol on the high-trans diet, while no change was observed in the low-trans group (mean treatment effect of 4´7 % (95 % CI 20´8, 10´5; P 0´10X No effects were found on total cholesterol and HDL-cholesterol, triacylglycerols, apolipoprotein B and A-1, and lipoprotein(a) concentrations. In conclusion, trans alinolenic acid may increase plasma LDL-:HDL-cholesterol and total cholesterol:HDL-cholesterol ratios. Whether diet-induced changes in these ratios truly affects the risk for CHD remains to be established.
Lipids, 1993
The effect of dietary a-linolenic acid (18:3n-3) and its ratio to linoleic acid (18:2n-6) on platelet and plasma phospholipid (PL) fatty acid patterns and prostanoid production were studied in normolipidemic men. The study consisted of two 42-d phases. Each was divided into a C~d pre-experimental period, during which a mixed fat diet was fed, and two 18-d experimental periods, during which a mixture of sunflower and olive oil [low 18:3n-3 content, high 18:2/18:3 ratio (LO-HI diet)], soybean oil (intermediate 18:3n-3 content, intermediate 18:2/18:3 ratio), canola oil (intermediate 18:3n-3 content, low 18:2/18:3 ratio) and a mixture of sunflower, olive and flax oil [high 18:3n~ content, low 18:2118:3 ratio (HI-LO diet)] provided 77% of the fat (26% of the energy) in the diet. The 18:3n-3 content and the 18:2/18:3 ratio of the experimental diets were: 0.8%,
Nutritional and metabolic effects of dietary trans fats depend on the intake of linoleic acid
European Journal of Lipid Science and Technology, 2015
This study aimed to investigate the differential effects of trans fatty acids (TFA) on the nutritional parameters, serum and tissue triacylglycerol (TAG) levels, as well as the mechanisms involved in their regulation, in male Wistar rats fed linoleic acid‐enriched (+LA) or LA‐deficient (−LA) diets. The TFA effects on nutritional parameters and TAG metabolism differed depending on the dietary LA status. In the +LA + TFA diet, compared to the +LA diet, TFA did not alter the serum TAG levels despite the increased epididymal adipose tissue (EAT) lipoprotein lipase (LPL) activity and the higher hepatic TAG content associated with a lower CPT‐Ia activity. Otherwise, in –LA + TFA rats versus −LA, TFA increased the serum, liver, and adipose tissue TAG levels associated with higher FAS, G6PDH, and ME enzyme activities in both liver and adipose tissue, and a reduced TAG clearance by the adipose tissue LPL enzyme. Although TFA supplementation in both –LA and +LA‐rats tended to decrease the CPT...
Associations of alpha-linolenic acid and linoleic acid with risk factors for coronary heart disease
2000
Background: Prevention of coronary heart disease (CHD) in high-risk subjects. Objective: To investigate the associations of dietary intake of alpha-linolenic acid (ALA) and linoleic acid (LA) as assessed by food frequency questionnaire and in the plasma cholesteryl ester (CE), with CHD risk factors. Design: Baseline data of a double-blind, randomized placebo-controlled trial. Subjects have hypercholesterolemia (6.0 ± 8.0 mmolal) and at least two other CHD risk factors (n 266). Results: The reported dietary ALA and LA intakes and the LAaALA ratio were associated with the contents in the CE (r 0.37, r 0.21, and r 0.42, respectively; P`0.01). In multivariate analysis, CE ALA was inversely associated with diastolic blood pressure (r 7 0.13; P`0.05) and positively with serum triacylglycerol (r 0.13; P`0.05), and CE LA was inversely associated with serum triacylglycerol (r 7 0.32; P`0.01). The CE LAaALA ratio was strongly inversely associated with CE ALA (r 7 0.95; P`0.01). In the lowest quintile of CE ALA, mean dietary intake was 0.4 energy % ALA (1.2 gaday), 8.4 energy % LA and an LAaALA ratio of 21, and in the highest quintile 0.6 energy % ALA (1.7 gaday), 6.8 energy % LA and 12 (ratio). In the lowest quintile of CE ALA the diastolic blood pressure was 4 mmHg lower (P trend`0.05), and the serum triacylglycerol 0.3 mmolal higher (P trend NS) when compared with the top quintile. Conclusions: In a CHD high-risk population with LA-rich background diet, these cross-sectional data suggest that replacing LA in the diet by ALA may decrease diastolic blood pressure, and may increase serum triacylglycerol concentration.
Dietary α-linolenic acid and health-related outcomes: a metabolic perspective
Nutrition Research Reviews, 2006
a-Linolenic acid (aLNA; 18 : 3n-3) is essential in the human diet, probably because it is the substrate for the synthesis of longer-chain, more unsaturated n-3 fatty acids, principally EPA (20 : 5n-3) and DHA (22 : 6n-3), which confer important biophysical properties on cell membranes and so are required for tissue function. The extent to which this molecular transformation occurs in man is controversial. The present paper reviews the recent literature on the metabolism of aLNA in man, including the use of dietary aLNA in b-oxidation, recycling of carbon by fatty acid synthesis de novo and conversion to longer-chain PUFA. Sex differences in aLNA metabolism and the possible biological consequences are discussed. Increased consumption of EPA and DHA in fish oil has a number of well-characterised beneficial effects on health. The present paper also reviews the efficacy of increased aLNA consumption in increasing the concentrations of EPA and DHA in blood and cell lipid pools, and the extent to which such dietary interventions might be protective against CVD and inflammation. Although the effects on CVD risk factors and inflammatory markers are variable, where beneficial effects have been reported these are weaker than have been achieved from increasing consumption of EPA þ DHA or linoleic acid. Overall, the limited capacity for conversion to longer-chain n-3 fatty acids, and the lack of efficacy in ameliorating CVD risk factors and inflammatory markers in man suggests that increased consumption of aLNA may be of little benefit in altering EPA þ DHA status or in improving health outcomes compared with other dietary interventions.
Current Developments in Nutrition, 2020
ABSTRACTBackgroundThe increased use of high-oleic oils to replace trans fat has led to concern about declining intake of PUFA and the potential for essential fatty acid insufficiency or even deficiency.ObjectivesThe aim of this study was to examine circulating concentrations of essential and poorly biosynthesized fatty acids, as biomarkers of dietary intake, in the NHANES data sets prior to (2003–2004 cycle) and following (2011–2012 cycle) legislation to reduce trans fat in the food supply and also to explore the associations between these fatty acids and markers of cardiometabolic health.MethodsFasting circulating concentrations of fatty acids from adults (aged ≥20 y) in the 2003–2004 and 2011–2012 NHANES cycles were used for analysis. Dietary data from one day of both the 2003–2004 and 2011–2012 cycles were used to examine differences in dietary fatty acid intake between these cycles. Regression analyses were used to assess relations between circulating concentrations of fatty aci...
Circulation, 2014
Previous studies on intake of linoleic acid (LA), the predominant n-6 fatty acid, and coronary heart disease (CHD) risk have generated inconsistent results. We performed a systematic review and meta-analysis of prospective cohort studies to summarize the evidence regarding the relation of dietary LA intake and CHD risk. We searched MEDLINE and EMBASE databases through June 2013 for prospective cohort studies that reported the association between dietary LA and CHD events. In addition, we used unpublished data from cohort studies in a previous pooling project. We pooled the multivariate-adjusted relative risk (RR) to compare the highest with the lowest categories of LA intake using fixed-effect meta-analysis. We identified 13 published and unpublished cohort studies with a total of 310 602 individuals and 12 479 total CHD events, including 5882 CHD deaths. When the highest category was compared with the lowest category, dietary LA was associated with a 15% lower risk of CHD events (p...
Journal of Nutrition, 2012
The c9,t11-18:2 isomer of conjugated linoleic acid (c9,t11-CLA) represents the main dietary CLA form with putative health benefits. Whereas CLA intake influences the tissue CLA concentration, little is known about the association between dietary CLA and the CLA content of plasma lipid fractions. This study was designed to document fasting and nonfasting plasma c9,t11-CLA concentrations in a population of free-living adults (n = 94) and relate these concentrations to c9,t11-CLA intake. We also determined the c9,t11-CLA content of the primary plasma lipid fractions in a subset (n = 50) of our participants, related these to c9,t11-CLA intake, and determined whether c9,t11-CLA intake or plasma c9,t11-CLA was correlated with plasma cholesterol. Mean fasting plasma c9,t11-CLA concentrations were 0.46 6 0.01 and 0.54 6 0.01% (wt:wt) of total fatty acids for men and women, respectively (P < 0.05); nonfasting concentrations were 0.28 6 0.01 and 0.38 6 0.01% of total fatty acids, respectively (P < 0.001). All major esterified plasma lipid fractions contained c9,t11-CLA; TG had the highest percentages. In men, c9,t11-CLA intake correlated (r = 0.47; P < 0.05) with TG c9,t11-CLA content, suggesting that TG c9,t11-CLA may serve as a biomarker for c9,t11-CLA intake. In females, there were no correlations between c9,t11-CLA intake and the c9,t11-CLA content of any esterified plasma lipid fraction. In neither sex was there a relation between dietary c9,t11-CLA or plasma c9,t11-CLA concentration and circulating lipoprotein cholesterol concentration. The influence of sex on circulating c9,t11-CLA content and further validation of biomarkers of c9,t11-CLA intake warrant further investigation.
The Journal of Nutrition, 2011
The usefulness of conjugated linoleic acid (CLA) as a nutraceutical remains ambiguous. Our objective was, therefore, to investigate the effect of CLA on body composition, blood lipids, and safety biomarkers in overweight, hyperlipidemic men. A double-blinded, 3-phase crossover trial was conducted in overweight (BMI $ 25 kg/m 2), borderline hypercholesterolemic [LDL-cholesterol (C) $ 2.5 mmol/L] men aged 18-60 y. During three 8-wk phases, each separated by a 4-wk washout period, 27 participants consumed under supervision in random order 3.5 g/d of safflower oil (control), a 50:50 mixture of trans 10, cis 12 and cis 9, trans 11 (c9, t11) CLA:Clarinol G-80, and c9, t11 isomer:c9, t11 CLA. At baseline and endpoint of each phase, body weight, body fat mass, and lean body mass were measured by DXA. Blood lipid profiles and safety biomarkers, including insulin sensitivity, blood concentrations of adiponectin, and inflammatory (high sensitive-C-reactive protein, TNFa, and IL-6) and oxidative (oxidized-LDL) molecules, were measured. The effect of CLA consumption on fatty acid oxidation was also assessed. Compared with the control treatment, the CLA treatments did not affect changes in body weight, body composition, or blood lipids. In addition, CLA did not affect the b-oxidation rate of fatty acids or induce significant alterations in the safety markers tested. In conclusion, although no detrimental effects were caused by supplementation, these results do not confirm a role for CLA in either body weight or blood lipid regulation in
The Journal of Nutrition, 2007
High linoleic acid (LA) intakes have been suggested to reduce a-linolenic acid [ALA, 18:3(n-3)] metabolism to eicosapentaenoic acid [EPA, 20:5(n-3)] and docosahexaenoic acid [DHA, 22:6(n-3)], and favor high arachidonic acid [ARA, 20:4(n-6)]. We used a randomized cross-over study with men (n ¼ 22) to compare the effect of replacing vegetable oils high in LA with oils low in LA in foods, while maintaining constant ALA, for 4 wk each, on plasma (n-3) fatty acids. Nonvegetable sources of fat, except fish and seafoods, were unrestricted. We determined plasma phospholipid fatty acids at wk 0, 2, 4, 6, and 8, and triglycerides, cholesterol, serum CRP, and IL-6, and platelet aggregation at wk 0, 4, and 8. LA and ALA intakes were 3.8 6 0.12% and 1.0 6 0.05%, and 10.5 6 0.53% and 1.1 6 0.06% energy with LA:ALA ratios of 4:0 and 10:1 during the low and high LA diets, respectively. The plasma phospholipid LA was higher and EPA was lower during the high than during the low LA diet period (P , 0.001), but DHA declined over the 8-wk period (r ¼ 20.425, P , 0.001). The plasma phospholipid ARA:EPA ratios were (mean 6 SEM) 20.7 6 1.52 and 12.9 6 1.01 after 4 wk consuming the high or low LA diets, respectively (P , 0.001); LA was inversely associated with EPA (r ¼ 20.729, P , 0.001) but positively associated with ARA:EPA (r ¼ 0.432, P , 0.001). LA intake did not influence ALA, ARA, DPA, DHA, or total, LDL or HDL cholesterol, CRP or IL-6, or platelet aggregation. In conclusion, high LA intakes decrease plasma phospholipid EPA and increase the ARA:EPA ratio, but do not favor higher ARA.