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PubMed1992

Volatile compound content and fatty acid composition of pork as influenced by linoleic acid content of the diet.

Eighty pigs (average weight of 60 kg) were allotted by weight and sex to pens and treatments. There were four dietary treatments, five pens per treatment, and four pigs per pen. Diets consisted of a typical corn-soybean mix containing 9% total fat, 3% from the corn-soybean mix and 6% added. The four dietary treatments included 1) 6% safflower oil, 2) 4% safflower oil and 2% tallow, 3) 2% safflower oil and 4% tallow, and 4) 6% tallow, resulting in 6.1, 4.6, 3.2, and 1.76% linoleic acid, respectively, in the diet. Pigs were slaughtered at an average weight of 100 kg. Proximate composition, tristimulus color coordinates (L, a, and b values), pH, and flavor difference of the longissimus muscle (LM) were evaluated. Fatty acid content (milligrams per 100 grams of tissue) of the subcutaneous fat and LM and headspace volatile content of the LM were determined by capillary gas liquid chromatography. Proximate composition, color, pH, and flavor of the LM were not influenced by diet. Fatty acid content of the subcutaneous fat and LM and volatile content of the LM were influenced by diet. Increased levels of safflower oil in the diet resulted in less C16:0 and C18:1 and more C18:2, C20:2, and C20:3 in the subcutaneous fat. The LM contained more C18:2 and less C18:3 and C24:0 due to increased levels of safflower oil in the diet. Compared with the 6% tallow diet, LM from pigs fed the 4 or 6% safflower diets contained more pentanal, hexanal, 2-heptanone, trans-2-heptenal, 2-pentyl furan, 2-ethyl-1-hexanol, decanal, and undecanal.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗
PubMed1988

Dietary linoleic acid and the fatty acid profiles in rats fed partially hydrogenated marine oils.

The influence of the linoleic acid levels of diets containing partially hydrogenated marine oils (HMO) rich in isomeric 16:1, 18:1, 20:1 and 22:1 fatty acids on the fatty acid profiles of lipids from rat liver, heart and adipose tissue was examined. Five groups of rats were fed diets containing 20 wt % fat--16% HMO + 4% vegetable oils. In these diets, the linoleic acid contents varied between 1.9% and 14.5% of the dietary fatty acids, whereas the contents of trans fatty acids were 33% in all groups. A sixth group was fed a partially hydrogenated soybean oil (HSOY) diet containing 8% linoleic acid plus 32% trans fatty acids, mainly 18:1, and a seventh group, 20% palm oil (PALM), with 10% linoleic acid and no trans fatty acids. As the level of linoleic acid in the HMO diets increased from 1.9% to 8.2%, the contents of (n-6) polyunsaturated fatty acids (PUFA) in the phospholipids increased correspondingly. At this dietary level of linoleic acid, a plateau in (n-6) PUFA was reached that was not affected by further increase in dietary 18:2 (n-6) up to 14.5%. Compared with the HSOY- or PALM-fed rats, the plateau values of 20:4(n-6) were considerably lower and the contents of 18:2(n-6) higher in liver phosphatidylcholines (PC) and heart PC. Heart phosphatidylethanolamines (PE) on the contrary, had elevated contents of 20:4(n-6), but decreased 22:5(n-6) compared with the PALM group.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗
PubMed2005

Dietary conjugated linoleic acid reduces lipid peroxidation by increasing oxidative stability in rats.

The antioxidative effect of conjugated linoleic acid (CLA) was examined by determining lipid peroxidation and antioxidative enzyme activities. Male Sprague-Dawley rats were fed one of the experimental diets-normal diet, vitamin E-deficient control diet, 0.5% CLA vitamin E-deficient diet, or 1.5% CLA vitamin E-deficient diet for 5 wk. Hepatic thiobarbituric acid reactive substances (TBARS) were increased in the vitamin E-deficient control group, but they were was significantly lowered in the CLA groups. Similarly, hepatic glutathione peroxidase activity was increased in the vitamin E-deficient diet and reduced by CLA supplementation. In addition, CLA caused a significant decrease in superoxide dismutase activity while having no effect on catalase activity. Analyses of the fatty acid composition revealed that dietary CLA was incorporated into hepatic microsomal membrane dose-dependently. Compared to the vitamin E-deficient control, CLA resulted in significantly higher saturated and monounsaturated fatty acids (palmitic and oleic acids) while lowering levels of oxidation-susceptible polyunsaturated fatty acids (linoleic, linolenic, and arachidonic acids) in both plasma and hepatic membrane. The concentrations of plasma cholesterol and triacylglycerol (TG) were lower in the 1.5% CLA group than in other groups. These results suggest that dietary CLA has antiatherosclerotic and antioxidant activity by increasing oxidative stability in plasma and hepatic membrane in the vitamin E-deficient rats.

Alanine Transaminase↗
PubMed1993

Escherichia coli produces linoleic acid during late stationary phase.

Escherichia coli produces linoleic acid in the late stationary phase. This was the case whether the cultures were grown aerobically or anaerobically on a supplemented glucose-salts medium. The linoleic acid was detected by thin-layer chromatography and was measured as the methyl ester by gas chromatography. The linoleic acid methyl ester was identified by its mass spectrum. Lipids extracted from late-stationary-phase cells generated thiobarbituric acid-reactive carbonyl products when incubated with a free radical initiator. In contrast, extracts from log-phase or early-stationary-phase cells failed to do so, in accordance with the presence of polyunsaturated fatty acid only in the stationary-phase cells.

Aerobiosis↗
PubMed1984

Further studies on the mechanism of increased blood pressure during dietary linoleic acid deprivation.

The present studies investigate the changes in blood pressure and excretory renal function in rats during dietary linoleic acid deprivation. Four groups of animals were fed isocaloric diets containing 10 en % saturated fat and either 5 en % linoleic acid (groups I and III) or 5 en % oleic acid (groups II and IV). In addition, groups I and II received a chronic high intake of Na (greater than 5 mmol/day) while groups III and IV were Na restricted with an average Na intake of 0.7 mumol/day. Blood pressure significantly increased in the high salt, linoleic acid deprived group II and was unchanged in all three other groups of animals. De novo synthesis of prostaglandin E2 in rat kidney inner medullary homogenates in the four groups of animals at the end of the dietary protocol showed a marked dependency on Na balance with significantly (p less than 0.01) higher values in the Na restricted animals as well as on linoleic acid intake with significantly (p less than 0.01) higher values in the linoleic acid substituted animals. Urinary excretion of NaCl during acute expansion of the extracellular fluid volume with hypotonic saline was significantly impaired in the animals receiving oleic acid instead of linoleic acid. In a metabolic study, linoleic acid deprived animals retained Na from the first day of linoleic acid deprivation and blood pressure started to rise only after a substantial amount of Na had been retained. Our results show that linoleic acid deprivation suppresses renal arachidonic acid cyclooxygenase metabolism and impairs the renal ability to excrete an acute salt load. Impaired renal excretory function precedes the increase in blood pressure. Thus suppressed renal cyclo-oxygenase metabolism which impairs renal excretory function may be a crucial mechanism in the rise of blood pressure during dietary linoleic acid deprivation.

Animals↗
PubMed1994

Linoleic acid uptake by isolated enterocytes: influence of alpha-linolenic acid on absorption.

In a previous study we showed that intestinal uptake of alpha-linolenic acid (18:3n-3) was carrier-mediated and we suggested that a plasma membrane fatty acid protein was involved in the transport of long-chain fatty acids. To further test this hypothesis, the mechanism of linoleic acid (18:2n-6) uptake by isolated intestinal cells was examined using a rapid filtration method and 20 mM sodium taurocholate as solubilizing agent. Under these experimental conditions transport of [1-14C]linoleic acid monomers in the concentration range of 2 to 2220 nM was saturable with a Vm of 5.1 +/- 0.6 nmol/mg protein/min and a Km of 183 +/- 7 nM. Experiments carried out in the presence of metabolic inhibitors, such as 2,4-dinitrophenol and antimycin A, suggested that an active, carrier-mediated mechanism was involved in the intestinal uptake of this essential fatty acid. The addition of excess unlabeled linoleic acid to the incubation medium led to a 89% decrease in the uptake of [1-14C]linoleic acid, while D-glucose did not compete for transport into the cell. Other long-chain polyunsaturated fatty acids added to the incubation mixture inhibited linoleic acid uptake by more than 80%. The presence of alpha-linolenic acid (18:3n-3) in the incubation medium caused the competitive inhibition (Ki = 353 nM) of linoleic acid uptake. The data are compatible with the hypothesis that intestinal uptake of both linoleic, and alpha-linolenic acid is mediated by a membrane carrier common to long-chain fatty acids.

Animals↗
PubMed2002

Differential effects of linoleic Acid metabolites on cardiac sodium current.

9,10-Epoxy-12-octadecenoic acid (EOA), a metabolite of linoleic acid, causes cardiac arrest in dogs. Other metabolites of linoleic acid also have toxic effects. This study investigates the mechanism of action of four of these compounds on cardiac Na(+) current (I(Na)). The whole-cell patch-clamp technique was used to investigate the effects of EOA, 9,10-dihydroxy-12-octadecenoic acid (DHOA), and their corresponding methyl esters (9,10-epoxy-12-octadecenoic methyl ester, EOM; and 9,10-dihydroxy-12-octadecenoic methyl ester, DHOM) on I(Na) in isolated adult rat ventricular myocytes. Extracellular application of each compound elicited a concentration-dependent inhibition of I(Na). The dose-response curve yielded 50% inhibition concentrations of 301 +/- 117 microM for DHOA, 41 +/- 6 microM for DHOM, 34 +/- 5 microM for EOA, and 160 +/- 41 microM for EOM. Although there was no effect on activation, 50 microM DHOM, EOA, and EOM significantly hyperpolarized the steady-state inactivation curve by approximately -6 mV. Furthermore, EOM significantly increased the slope of the steady-state inactivation curve. These compounds also seemed to stabilize the inactivated state because the time for recovery from inactivation was significantly slowed from a control value of 12.9 +/- 0.5 ms to 30.5 +/- 3.3, 31.4 +/- 1.4, and 20.5 +/- 1.0 ms by 50 microM DHOM, EOA, and EOM, respectively. These compounds have multiple actions on Na(+) channels and that despite their structural similarities their actions differ from each other. The steady-state block of I(Na) suggests that either the pore is being blocked or the channels are prevented from gating to the open state. In addition, these compounds stabilize the inactivated state and promote increased population of a slower inactivated state.

Animals↗
PubMed1982

Enrichment of human platelet phospholipids with linoleic acid diminishes thromboxane release.

We have investigated whether exposure of human platelets to elevated concentrations of linoleic acid, the principal dietary polyunsaturate, would influence platelet thromboxane A2 release. Platelets were incubated with albumin-bound linoleic acid at 30 degrees C for 24 h, with prostaglandin E1 added to prevent aggregation. The linoleic acid supplemented platelets released, on average, 50% less thromboxane A2 in response to stimulation with thrombin than corresponding control platelets. Other fatty acids were without appreciable effect. The inhibition of thrombin-stimulated thromboxane A2 release was dependent on the time and temperature of incubation, as well as on the concentration of added linoleic acid. Supplementation increased the amount of linoleic acid in the platelet phospholipids, but the arachidonic acid content of the phospholipids was reduced. [1-14C]Linoleic acid was not converted to arachidonic acid by the platelets. Linoleic acid was released exclusively from the inositol phosphoglycerides when the enriched platelets were stimulated with thrombin. The linoleate-enriched platelets converted less [1-14C]arachidonic acid to all prostaglandin products, suggesting that the platelet cyclooxygenase was partially inhibited.

Arachidonic Acid↗
PubMed2006

Conjugated linoleic acid: a functional nutrient in the different pathophysiological components of the metabolic syndrome?

PURPOSE OF REVIEW: Much attention has focused on the therapeutic potential of conjugated linoleic acid with the most abundant isomers being cis-9,trans-11 conjugated linoleic acid and trans-10,cis-12 conjugated linoleic acid. Initial animal studies associated conjugated linoleic acid with beneficial health properties, such as reducing the risk of cancer, diabetes, atherosclerosis, inflammation and obesity. This review has appraised the evidence in relation to the effect of conjugated linoleic acid on components of the metabolic syndrome (clinically or experimentally), in particular, obesity, insulin resistance, atherosclerosis and inflammation. RECENT FINDINGS: More recent human conjugated linoleic acid supplementation studies have often shown conflicting and less convincing health benefits. The marked variation between studies may reflect the isomer-specific effect of the individual conjugated linoleic acid isomers, which can often have opposing effects. Detrimental effects have been observed in some studies, in particular after supplementation with the trans-10,cis-12 conjugated linoleic acid isomer. SUMMARY: Further studies and long-term clinical trials will be required to determine the efficacy and safety of conjugated linoleic acid isomers before conjugated linoleic acid could be considered as a functional nutrient in humans.

Atherosclerosis↗
PubMed1999

Comparison of bolus versus fractionated oral applications of [13C]-linoleic acid in humans.

BACKGROUND: The endogenous conversion of linoleic acid into long-chain polyunsaturated fatty acids is of potential importance for meeting substrate requirements, particularly in young infants. After application of [13C]-linoleic acid, we estimated its conversion to dihomo-gamma-linolenic and arachidonic acids from only two blood samples. DESIGN: Oral tracer doses were given to five healthy adults as a single bolus. In four subjects the tracer was given in nine equal portions over 3 days. Concentration and 13C content of fatty acids from serum phospholipids were analysed by gas chromatography combustion isotope ratio-mass spectrometry. Areas under the tracer-concentration curves were calculated, and fractional transfer and turnover rates estimated from compartmental models. RESULTS: The median fractional turnover of linoleic acid was 93.7% per day (interquartile range 25.3) in the bolus group and 80. 0% per day (6.3) in the fraction group (NS). Fractional conversion of linoleic to dihomo-gamma-linolenic acid was 1.5% (0.9) vs. 2.1% (0.7) (bolus vs. fraction, P < 0.05), and fractional conversion of linoleic to arachidonic acid was 0.3% (0.3) vs. 0.6% (0.3) (bolus vs. fraction, NS). In the fraction group conversion was significantly higher based on areas under the curve. The ratio of tracer concentration in conversion products to linoleic acid 48 h after dosing correlated very well (r >/= 0.94, P < 0.05) with the ratio of areas under the curve. CONCLUSIONS: Using areas under the curve overestimates the conversion, because different residence times are not considered. Estimation of conversion intensity appears possible with only one blood sample obtained after tracer application.

8,11,14-Eicosatrienoic Acid↗
PubMed2001

Mitochondrial respiration on rumenic and linoleic acids.

Rumenic acid (cis-9, trans-11-C(18:2)) represents approx. 80% of conjugated linoleic acid (CLA) in dairy products. CLA has been shown to exert beneficial effects on health, but little work has been devoted to the ability to oxidize CLA isomers and the role of these isomers in the modulation of beta-oxidation flux. In the present study, respiration on rumenic acid was compared with that on linoleic acid (cis-9, cis-12-C(18:2)) with the use of rat liver mitochondria. In state-3, respiration was decreased by half with rumenic acid in comparison with linoleic acid. In the uncoupled state, respiration on CLA remained 30% lower. The lower ability to oxidize CLA was investigated through characterization of the enzymic steps. Rumenic acid was 33% less activated by acyl-CoA synthase than was linoleic acid. However, after such activation, the transfer of both acyl moieties to carnitine by carnitine acyltransferase I (CAT I) was of the same order. Moreover, CAT II activity was comparable with either isomer. After prior incubation with rumenic acid, oxidation of octanoic acid by re-isolated mitochondria was unimpaired, but that of palmitoleic acid was impaired unless linoleic acid was used in the prior incubation. The slower respiration on cis-9, trans-11-C(18:2) is suggested to arise from lower carnitine-acylcarnitine translocase activity towards the acylcarnitine form, causing an upstream increase in the corresponding acyl-CoA.

Animals↗
PubMed2003

Analysis of oxidative DNA damage after human dietary supplementation with linoleic acid.

It has been hypothesized that oxygen radicals generated by peroxidation of dietary linoleic acid may induce genetic damage and thereby increase cancer risk. We examined the effect of dietary supplementation with linoleic acid on the levels of oxidative DNA damage in peripheral lymphocytes and on the blood plasma antioxidant potential. Thirty volunteers received during 6 weeks either a high dose of linoleic acid (15 g/day), an intermediate dose of linoleic acid (7.5 g/day) or an isocaloric supplement without linoleic acid (15 g palmitic acid/day). After the intervention, no significant increase in oxidative DNA damage, measured as relative amounts of 7,8-dihydro-8-oxo-2'-deoxyguanosine (8-oxodG) in DNA from peripheral lymphocytes, was observed in both high and intermediate linoleic acid-supplemented groups (increase of respectively 13 and 21%; P>0.05). Also, the differences between levels of oxidative DNA damage in the high or intermediate linoleic acid-supplemented group and the control group receiving palmitic acid (23% decrease) were not significant. Furthermore, no statistically significant differences were found between the total antioxidant capacities of blood plasma from the different experimental groups. Plasma levels of malondialdehyde, an important end-product of lipid peroxidation, were not increased after supplementation, nor were effects found on the plasma concentrations of retinol, alpha-tocopherol and beta-carotene. Despite the experimental design that excludes several forms of bias introduced in studies based on modulation of dietary composition, our results provide no indication of increased oxidative stress or genetic damage as a result of increased dietary intake of linoleic acid. Therefore, we see no scientific basis to reconsider the public health policy to stimulate the intake of polyunsaturated fatty acids aimed at the reduction of coronary heart diseases.

Adult↗
PubMed1996

Low concentrations of cis-linoleic acid induce cell damage in epithelial cells from bovine lenses.

As low as 5 micromol/l of cis-linoleic acid proves to be cytotoxic for bovine lens epithelial cells in culture. Albumin eliminates the linoleic acid cytotoxicity completely, presumably by binding the fatty acid. However, the damaging effect appears again when the molar ratio of linoleic acid to albumin exceeds 1:1. The assumption that the linoleic acid-caused cell damage would be mediated by peroxidation products could not be confirmed. The results obtained rather favor the idea that linoleic acid molecules themselves injure lens epithelial cells. Obviously, cell damage even occurs in the presence of albumin if one molecule of albumin binds more than one molecule of linoleic acid. Micromolar concentrations of linoleic acid produce reversible bleb formation as well as cell retraction within 30 min. In primary culture 10 micromol/l linoleic acid damage lens epithelial cells irreversibly within some hours. Trans-linoleic acid, linolenic acid and oleic acid are also harmful to lens cells but to a lesser degree, while saturated fatty acids are without any effect. Bleb formation as a leading early sign hints at the plasma membrane as the primary target for linoleic acid induced cytotoxicity.

Albumins↗
PubMed1989

Soybean lipoxygenase-1 enzymically forms both (9S)- and (13S)-hydroperoxides from linoleic acid by a pH-dependent mechanism.

Soybean lipoxygenase-1 produces a preponderance of two chiral products from linoleic acid, (13S)-(9Z,11E)-13-hydroperoxy-9,11-octadecadienoic acid and (9S)-(10E,12Z)-9-hydroperoxy-10,12-octadecadienoic acid. The former of these hydroperoxides was generated at all pH values, but in the presence of Tween 20, the latter product did not form at pH values above 8.5. As the pH decreased below 8.5, the proportion of (9S)-hydroperoxide increased linearly until at pH 6 it constituted about 25% of the chiral products attributed to enzymic action. Below pH 6, lipoxygenase activity was barely measurable, and the hydroperoxide product arose mainly from autoxidation and possibly non-enzymic oxygenation of the pentadienyl radical formed by the enzyme. The change in percent enzymically formed 9-hydroperoxide between pH 6.0 and 8.5 paralleled the pH plot of a sodium linoleate/linoleic acid titration. It was concluded that the (9S)-hydroperoxide is formed only from the nonionized carboxylic acid form of linoleic acid. Methyl esterification of linoleic acid blocked the formation of the (9S)-hydroperoxide by lipoxygenase-1, but not the (13S)-hydroperoxide. Since the hydroperoxydiene moieties of the (9S)- and (13S)-hydroperoxides are spatially identical when the molecules are arranged head to tail in opposite orientations, it is suggested that the carboxylic acid form of the substrate can arrange itself at the active site in either orientation, but the carboxylate anion can be positioned only in one orientation. These observations, as well as others in the literature, suggest and active-site model for soybean lipoxygenase-1.

Binding Sites↗
PubMed1993

Can linoleic acid contribute to coronary artery disease?

The adipose tissue concentration of linoleic acid was positively associated with the degree of coronary artery disease (CAD) in a cross-sectional study of 226 patients undergoing coronary angiography. Linoleic acid concentration in adipose tissue is known to reflect the intake of this fatty acid. These results are therefore indicative of a positive relationship between linoleic acid intake and CAD. The platelet linoleic acid concentration was also positively associated with CAD. After confounding factors were allowed for, the eicosapentaenoic acid concentration in platelets was inversely associated with CAD for men, and the docosapentaenoic acid concentration in platelets was inversely associated with CAD for women; results consistent with several other studies that suggest that fish, and omega-3 fatty acids derived from fish and fish oils, can beneficially influence macrovascular disease.

Adipose Tissue↗
PubMed2007

The alteration of plasminogen activator inhibitor-1 expression by linoleic acid and fenofibrate in HepG2 cells.

The present study investigated the influence of linoleic acid and fenofibrate on plasminogen activator inhibitor-1 (PAI-1) expression in HepG2 cells and the mechanism possibly involved. Using gene recombination techniques, chloromycetin acetyltransferase (CAT) reporter gene plasmids containing nuclear factor-kappaB response element deletion (del1-PAI-pCAT) or very-low-density lipoprotein/fatty acid response element deletion (del2-PAI-pCAT) in the PAI-1 promoter were constructed and transiently transfected into HepG2 cells, respectively. Linoleic acid and fenofibrate were added to induce the transfected cells. The PAI-1 expression in mRNA and protein level was significantly induced by linoleic acid, but suppressed by fenofibrate. In the HepG2 cells transfected with PAI-pCAT plasmid, the PAI-1 transcription activity was significantly induced by linoleic acid, but suppressed by fenofibrate. Under transfection with del1-PAI-pCAT, both linoleic acid and fenofibrate increased the PAI-1 transcriptional activity; whereas in those cells transfected with del2-PAI-pCAT, fenofibrate significantly reduced PAI-1 transcriptional activity but no change was found with linoleic acid stimulation. Peroxisome proliferator-activated receptor alpha may be one of transcription factors playing a role in the upregulation of PAI-1 gene expression by linoleic acid in HepG2 cells. The inhibition of the nuclear factor-kappaB signaling pathway may be involved in the downregulation of PAI-1 gene expression by fenofibrate.

Cell Line, Tumor↗
PubMed2005

Attenuation of breast tumor cell growth by conjugated linoleic acid via inhibition of 5-lipoxygenase activating protein.

Conjugated linoleic acid (CLA) consists of a group of linoleic acid geometric isomers that have been shown to reduce tumor growth and metastasis in animal models of breast, prostate and colon cancer. To delineate a possible mechanism of action for CLA, we have recently shown that the 5-lipoxygenase product, 5-hydroxyeicosatetraenoic acid (5-HETE), could play a role in CLA alteration of mammary tumorigenesis. In this study, we determined how CLA could modulate 5-lipoxygenase activity. The t10, c12-CLA isomer reduced production of 5-HETE but not 12- and 15-HETE in MDA-MB-231 human breast tumor cells. That isomer and the c9, t11-CLA isomer decreased 5-HETE production by competition with the lipoxygenase substrate, arachidonic acid (AA). Interestingly, t10, c12-CLA reduced the expression of five-lipoxygenase activating protein (FLAP) but not the 5-lipoxygenase enzyme. Over-expression of FLAP abrogated t10, c12-CLA-reduced viability of MDA-MB-231 cells. These data suggest that the reduction of 5-HETE by t10, c12-CLA was due to competition with AA and the reduction of FLAP expression.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1985

Serum linoleic acid and cardiovascular death in postinfarction middle-aged men.

Linoleic acid in serum total lipids was the first variable in the stepwise regression analysis of metabolic, nutritional and cardiovascular factors in a secondary preventive study of postinfarction middle-aged men. It was followed in the regression analysis where the dependent variable was cardiovascular death by previous myocardial infarction, heart volume index and hyperlipoproteinaemia. Linoleic acid was the only fatty acid entering the regression. Unlike other fatty acids, it exhibited by its low percentage an accumulation of deaths. The decreased percentage of linoleic acid was also evident in the comparison of fatty acid patterns of cardiovascular deaths to age- and triglyceride-matched men free from ischaemic heart disease. This study confirms prospective associations found in previously healthy men. Conclusions are drawn about the relevance of low serum linoleic acid to long term prognosis after MI.

Cardiovascular Diseases↗