linoleic-acid and Myocardial-Infarction

To examine the traditional diet-heart hypothesis through recovery and analysis of previously unpublished data from the Minnesota Coronary Experiment (MCE) and to put findings in the context of existing diet-heart randomized controlled trials through a systematic review and meta-analysis.. The MCE (1968-73) is a double blind randomized controlled trial designed to test whether replacement of saturated fat with vegetable oil rich in linoleic acid reduces coronary heart disease and death by lowering serum cholesterol. Recovered MCE unpublished documents and raw data were analyzed according to hypotheses prespecified by original investigators. Further, a systematic review and meta-analyses of randomized controlled trials that lowered serum cholesterol by providing vegetable oil rich in linoleic acid in place of saturated fat without confounding by concomitant interventions was conducted.. One nursing home and six state mental hospitals in Minnesota, United States.. Unpublished documents with completed analyses for the randomized cohort of 9423 women and men aged 20-97; longitudinal data on serum cholesterol for the 2355 participants exposed to the study diets for a year or more; 149 completed autopsy files.. Serum cholesterol lowering diet that replaced saturated fat with linoleic acid (from corn oil and corn oil polyunsaturated margarine). Control diet was high in saturated fat from animal fats, common margarines, and shortenings.. Death from all causes; association between changes in serum cholesterol and death; and coronary atherosclerosis and myocardial infarcts detected at autopsy.. The intervention group had significant reduction in serum cholesterol compared with controls (mean change from baseline -13.8%v-1.0%; P<0.001). Kaplan Meier graphs showed no mortality benefit for the intervention group in the full randomized cohort or for any prespecified subgroup. There was a 22% higher risk of death for each 30 mg/dL (0.78 mmol/L) reduction in serum cholesterol in covariate adjusted Cox regression models (hazard ratio 1.22, 95% confidence interval 1.14 to 1.32; P<0.001). There was no evidence of benefit in the intervention group for coronary atherosclerosis or myocardial infarcts. Systematic review identified five randomized controlled trials for inclusion (n=10,808). In meta-analyses, these cholesterol lowering interventions showed no evidence of benefit on mortality from coronary heart disease (1.13, 0.83 to 1.54) or all cause mortality (1.07, 0.90 to 1.27).. Available evidence from randomized controlled trials shows that replacement of saturated fat in the diet with linoleic acid effectively lowers serum cholesterol but does not support the hypothesis that this translates to a lower risk of death from coronary heart disease or all causes. Findings from the Minnesota Coronary Experiment add to growing evidence that incomplete publication has contributed to overestimation of the benefits of replacing saturated fat with vegetable oils rich in linoleic acid.

Topics: Adult; Aged; Aged, 80 and over; Cause of Death; Cholesterol; Coronary Artery Disease; Coronary Disease; Diet, Fat-Restricted; Dietary Fats; Double-Blind Method; Female; History, 20th Century; Humans; Kaplan-Meier Estimate; Linoleic Acid; Male; Middle Aged; Minnesota; Myocardial Infarction; Plant Oils; Randomized Controlled Trials as Topic; Risk Factors; Young Adult

Randomised controlled trials (RCT) of mixed n-6 and n-3 PUFA diets, and meta-analyses of their CHD outcomes, have been considered decisive evidence in specifically advising consumption of 'at least 5-10 % of energy as n-6 PUFA'. Here we (1) performed an extensive literature search and extracted detailed dietary and outcome data enabling a critical examination of all RCT that increased PUFA and reported relevant CHD outcomes; (2) determined if dietary interventions increased n-6 PUFA with specificity, or increased both n-3 and n-6 PUFA (i.e. mixed n-3/n-6 PUFA diets); (3) compared mixed n-3/n-6 PUFA to n-6 specific PUFA diets on relevant CHD outcomes in meta-analyses; (4) evaluated the potential confounding role of trans-fatty acids (TFA). n-3 PUFA intakes were increased substantially in four of eight datasets, and the n-6 PUFA linoleic acid was raised with specificity in four datasets. n-3 and n-6 PUFA replaced a combination of TFA and SFA in all eight datasets. For non-fatal myocardial infarction (MI)+CHD death, the pooled risk reduction for mixed n-3/n-6 PUFA diets was 22 % (risk ratio (RR) 0.78; 95 % CI 0.65, 0.93) compared to an increased risk of 13 % for n-6 specific PUFA diets (RR 1.13; 95 % CI 0.84, 1.53). Risk of non-fatal MI+CHD death was significantly higher in n-6 specific PUFA diets compared to mixed n-3/n-6 PUFA diets (P = 0.02). RCT that substituted n-6 PUFA for TFA and SFA without simultaneously increasing n-3 PUFA produced an increase in risk of death that approached statistical significance (RR 1.16; 95 % CI 0.95, 1.42). Advice to specifically increase n-6 PUFA intake, based on mixed n-3/n-6 RCT data, is unlikely to provide the intended benefits, and may actually increase the risks of CHD and death.

Topics: Coronary Disease; Dietary Fats; Fatty Acids, Omega-3; Fatty Acids, Omega-6; Humans; Linoleic Acid; Myocardial Infarction; Randomized Controlled Trials as Topic; Risk Factors

Since the discovery in 1929 that certain polyunsaturated fatty acids (PUFA) are essential for life and health, intense investigation has revealed the multiplicity of members in each of several families of PUFA, no two of which are equivalent. The quantified nutrient requirements for the essential dietary precursors of the two dominant families of PUFA have been estimated, and the general functions of these families are slowly becoming known. The PUFA are essential components of structural membrane lipids. The functions of the individual members are not yet differentiated, except as they act as precursors of synthesis of unique octadecanoid, eicosanoid, and docosanoid products of oxidation that have potent biological properties. The PUFA occur in animals and higher plants as ubiquitous and essential components of structural lipid that are in a dynamic equilibrium with the pool of dietary acyl groups. Many human diseases have been found to involve unique essential fatty acid (EFA) deficiencies or distortions of the normal equilibrium pattern. The equilibrium is influenced by the level of dietary intake or precursors, by the presence of competing essential and nonessential acyl groups, by nonoptimum intake of other essential nutrients, by hormonal effects, by drug therapy, and by other effects upon physiological condition. With the many variables already known to modulate or control the equilibrium, it should be possible with more precise understanding of each variable to shift abnormal equilibria in the direction of normalcy. This perhaps will be the next area of intensive investigation in this field of nutrition and metabolism.

Topics: Acrodermatitis; alpha-Linolenic Acid; Arachidonic Acid; Arachidonic Acids; Aspirin; Child; Crohn Disease; Cystic Fibrosis; DDT; Dicofol; Ethanol; Fatty Acids, Essential; Fatty Acids, Unsaturated; Female; Humans; Ichthyosis; Indomethacin; Isomerism; Linoleic Acid; Linoleic Acids; Linolenic Acids; Lipid Metabolism; Lipolysis; Liver Cirrhosis, Alcoholic; Models, Chemical; Myocardial Infarction; Protein-Energy Malnutrition; Reye Syndrome; Structure-Activity Relationship

Dihomo-gamma-linolenic acid (DGLA) is an

Topics: 8,11,14-Eicosatrienoic Acid; Aged; Female; Humans; Kaplan-Meier Estimate; Linoleic Acid; Male; Multivariate Analysis; Myocardial Infarction; Phospholipids; Proportional Hazards Models

The double-blind OMEGA-REMODEL placebo-controlled randomized trial of high-dose omega-3 fatty acids (O-3FA) post-acute myocardial infarction (AMI) reported improved cardiac remodeling and attenuation of non-infarct myocardial fibrosis. Fatty acid desaturase 2 (FADS2) gene cluster encodes key enzymes in the conversion of essential omega-3 and omega-6 fatty acids into active arachidonic (ArA) and eicosapentaenoic acids (EPA), which influence cardiovascular outcomes.. We tested the hypothesis that the genotypic status of FADS2 (rs1535) modifies therapeutic response of O-3FA in post-AMI cardiac remodeling in 312 patients. Consistent with known genetic polymorphism of FADS2, patients in our cohort with the guanine-guanine (GG) genotype had the lowest FADS2 activity assessed by arachidonic acid/linoleic acid (ArA/LA) ratio, compared with patients with the adenine-adenine (AA) and adenine-guanine (AG) genotypes (GG:1.62±0.35 vs. AA: 2.01±0.36, p<0.0001; vs. AG: 1.76±0.35, p = 0.03). When randomized to 6-months of O-3FA treatment, GG patients demonstrated significant lowering of LV end-systolic volume index (LVESVi), N-terminal prohormone of brain natriuretic peptide (NT-proBNP), and galectin-3 levels compared to placebo (-4.4 vs. 1.2 ml/m2, -733 vs. -181 pg/mL, and -2.0 vs. 0.5 ng/mL; p = 0.006, 0.006, and 0.03, respectively). In contrast, patients with either AA or AG genotype did not demonstrate significant lowering of LVESVi, NT-proBNP, or galectin-3 levels from O-3FA treatment, compared to placebo. The odds ratios for improving LVESVi by 10% with O-3FA treatment was 7.2, 1.6, and 1.2 in patients with GG, AG, and AA genotypes, respectively.. Genetic profiling using FADS2 genotype can predict the therapeutic benefits of O-3FA treatment against adverse cardiac remodeling during the convalescent phase of AMI.. clinicaltrials.gov Identifier: NCT00729430.

Topics: Aged; Arachidonic Acid; Double-Blind Method; Fatty Acid Desaturases; Fatty Acids, Omega-3; Female; Humans; Linoleic Acid; Male; Middle Aged; Myocardial Infarction; Pharmacogenomic Variants; Polymorphism, Single Nucleotide; Prospective Studies; Tertiary Care Centers; Treatment Outcome; Ventricular Remodeling

Total and individual plasma free fatty acids (FFA) were measured on admission and over the next 4 days in 24 patients admitted to the hospital with chest pain and suspected acute myocardial infarction (AMI). In a prospective randomized fashion, the patients were either given an infusion of 300 gm of glucose, 50 units of insulin, and 80 mEq of KCl per liter at a rate of 1.5 ml/kg/hr over the initial 48 hours of hospitalization, or they served as controls receiving conventional therapy. Eleven patients were in the control group and 13 were in the glucose-insulin-potassium (G-I-K) group. Twenty-one of the patients had an AMI by CK-MB rise and ECG changes (in the G-I-K group three did not evolve AMI). The total plasma FFA were 840 +/- 134 microM/L in the controls and 933 +/- 160 microM/L in the G-I-K group initially (prestudy). Total FFA rapidly fell in the G-I-K group and then rebounded when G-I-K was stopped. In contrast, total FFA values fell gradually in the control group over the 4-day period. The individual FFA had similar percentages initially in the two groups. In the control group the percent of individual plasma FFA was unchanged over the period studied, although there was some mild random day-to-day fluctuation. In contrast in the G-I-K group linoleic acid fell both during and after the infusion was stopped (26.8% to 19.1% P less than 0.001). Arachidonic acid doubled in percentage of the total FFA value during G-I-K infusion (3.1% to 6.5%, P less than 0.002) and returned to the control value when it was stopped. Thus G-I-K infusion during AMI reduces the total level of plasma FFA while increasing the percent of arachidonic and decreasing the percent of linoleic acid, observations proposed to reflect improved membrane stability of the ischemic myocardium.

Topics: Acute Disease; Adult; Aged; Arachidonic Acid; Arachidonic Acids; Clinical Trials as Topic; Fatty Acids, Nonesterified; Female; Glucose; Humans; Infusions, Parenteral; Insulin; Linoleic Acid; Linoleic Acids; Male; Middle Aged; Myocardial Infarction; Potassium; Prospective Studies; Random Allocation

Primary ventricular fibrillation (PVF) is a major driver of cardiac arrest in the acute phase of ST-segment elevation myocardial infarction (STEMI). Enrichment of cardiomyocyte plasma membranes with dietary polyunsaturated fatty acids (PUFA) reduces vulnerability to PVF experimentally, but clinical data are scarce. PUFA status in serum phospholipids is a valid surrogate biomarker of PUFA status in cardiomyocytes within a wide range of dietary PUFA. In this nested case-control study (n = 58 cases of STEMI-driven PVF, n = 116 control non-PVF STEMI patients matched for age, sex, smoking status, dyslipidemia, diabetes mellitus and hypertension) we determined fatty acids in serum phospholipids by gas-chromatography, and assessed differences between cases and controls, applying the Benjamini-Hochberg procedure on nominal P-values to control the false discovery rate (FDR). Significant differences between cases and controls were restricted to linoleic acid (LA), with PVF patients showing a lower level (nominal P = 0.002; FDR-corrected P = 0.027). In a conditional logistic regression model, each one standard deviation increase in the proportion of LA was related to a 42% lower prevalence of PVF (odds ratio = 0.58; 95% confidence interval, 0.37, 0.90; P = 0.02). The association lasted after the inclusion of confounders. Thus, regular consumption of LA-rich foods (nuts, oils from seeds) may protect against ischemia-driven malignant arrhythmias.

Topics: Case-Control Studies; Fatty Acids, Unsaturated; Humans; Linoleic Acid; Myocardial Infarction; Phospholipids; ST Elevation Myocardial Infarction; Ventricular Fibrillation

We investigated risk of myocardial infarction (MI) associated with the content of linoleic acid (LA) in adipose tissue, a biomarker of long-term dietary intake of LA and a marker of endogenous LA exposure.. Between 1993 and 1997, 57,053 middle-aged subjects were included in the Danish Diet, Cancer and Health cohort. We performed a case-cohort study that included a random sample of the full cohort (n = 3167) and all incident MI cases appearing during 16 years of follow-up (n = 2819). Information on incident MI cases was obtained by linkage with Danish nationwide registries. Adipose tissue biopsies were taken from the buttocks of the participants, and their fatty acid composition was determined using gas chromatography. HRs (hazard ratios) with 95% confidence intervals (CIs) were used to describe the associations between content of LA in adipose tissue and the risk of MI. HRs were calculated using weighted Cox proportional hazards regression with robust variance.. After adjustment for established risk factors of MI, adipose tissue content of LA was not associated with the risk of MI in men and women combined (quintiles 5 versus 1, HR, 1.03 (95% CI, 0.85-1.25), P-trend = 0.970) or in men and women separately (quintiles 5 versus 1, HR, 1.05 (95% CI, 0.83-1.33), P-trend = 0.871 and quintiles 5 versus 1, HR, 0.99 (95% CI 0.72-1.37), P-trend = 0.928, respectively). Investigating the association between LA and MI with a shorter, 5- or 10-year duration of follow-up provided similar results.. Content of LA in adipose tissue was not associated with the risk of MI.

Topics: Adipose Tissue; Cohort Studies; Female; Humans; Linoleic Acid; Male; Middle Aged; Myocardial Infarction; Risk Factors

To study plasma and dietary linoleic acid (LA) in relation to type 2 diabetes risk in post-myocardial infarction (MI) patients.. We included 3,257 patients aged 60-80 years (80% male) with a median time since MI of 3.5 years from the Alpha Omega Cohort and who were initially free of type 2 diabetes. At baseline (2002-2006), plasma LA was measured in cholesteryl esters, and dietary LA was estimated with a 203-item food-frequency questionnaire. Incident type 2 diabetes was ascertained through self-reported physician diagnosis and medication use. Hazard ratios (with 95% CIs) were calculated by Cox regressions, in which dietary LA isocalorically replaced the sum of saturated (SFA) and. Mean ± SD circulating and dietary LA was 50.1 ± 4.9% and 5.9 ± 2.1% energy, respectively. Plasma and dietary LA were weakly correlated (Spearman. In our cohort of post-MI patients, plasma LA was inversely related to type 2 diabetes risk, whereas dietary LA was not related. Further research is needed to assess whether plasma LA indicates metabolic state rather than dietary LA in these patients.

Topics: Aged; Aged, 80 and over; Biomarkers; Cohort Studies; Diabetes Mellitus, Type 2; Diet; Dietary Fats; Female; Follow-Up Studies; Humans; Linoleic Acid; Male; Middle Aged; Myocardial Infarction; Nutrition Surveys; Prospective Studies; Risk Factors; Trans Fatty Acids

Population-based studies often use plasma fatty acids (FAs) as objective indicators of FA intake, especially for n-3 FA and linoleic acid (LA). The relation between dietary and circulating FA in cardiometabolic patients is largely unknown. We examined whether dietary n-3 FA and LA were reflected in plasma lipid pools in post-myocardial infarction (MI) patients.. Patients in Alpha Omega Cohort filled out a 203-item food-frequency questionnaire from which eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), alpha-linolenic acid (ALA), and LA intake were calculated. Circulating individual FA (% total FA) were assessed in cholesteryl esters (CE; n = 4066), phospholipids (PL; n = 838), and additionally in total plasma for DHA and LA (n = 739). Spearman correlation coefficients (r. In post-MI patients, dietary EPA and DHA were well reflected in circulating levels. This was not the case for LA, which may partly be influenced by alcohol use and statins.

Topics: Aged; Aged, 80 and over; Alcohol Drinking; Biomarkers; Cross-Sectional Studies; Diet Records; Docosahexaenoic Acids; Eicosapentaenoic Acid; Feeding Behavior; Female; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Linoleic Acid; Male; Middle Aged; Myocardial Infarction; Netherlands; Prospective Studies

We previously observed that resolvin D1 (RvD1), a metabolite of the omega-3 polyunsaturated fatty acid (PUFA) docosahexaenoic acid, reduces infarct size by a mechanism involving the PI3-K/Akt pathway. In parallel, the beneficial effect of a high omega-3 PUFA diet on infarct size can be attenuated by increased omega-6 PUFA consumption. The present study was designed to determine if augmented linoleic acid (LA), an omega-6 PUFA administered at the same time, attenuates the cardioprotective action of RvD1. Male Sprague-Dawley rats received 0.1μg RvD1 alone or with one of three LA doses (1, 5 or 10μg) directly into the left ventricle chamber 5min before ischemia. The animals underwent 40min of ischemia by occlusion of the left descending coronary artery followed by 30min or 24h of reperfusion. Infarct size and neutrophil accumulation were evaluated after 24h of reperfusion, while caspase-3, -8 and -9 and Akt activities were assessed at 30min of reperfusion. LA attenuated cardioprotection afforded by RvD1, resulting in significantly increased infarct size. Neutrophil accumulation and Akt activity were similar between groups. Caspase activities, especially caspase-9, which could be activated by ischemia, were stimulated in the presence of LA, suggesting that this omega-6 PUFA accentuates ischemia intensity. The present results indicate that LA significantly attenuates the beneficial effect of RvD1 on infarct size. Therefore, reduction of omega-6 intake should be considered to maintain the protection afforded by RvD1.

Topics: Animals; Body Weight; Cardiotonic Agents; Caspases; Docosahexaenoic Acids; Hemodynamics; Linoleic Acid; Myocardial Infarction; Rats; Rats, Sprague-Dawley

Although fatty acid intake has been associated with risk of coronary disease events, the association between blood omega-6 and trans fatty acids (FAs) at the time of an acute coronary syndrome (ACS) is unknown.. The relationship of blood FA composition to ACS was analyzed in 768 incident cases and 768 controls (matched on age, sex, and race).. Compared to controls, ACS cases' blood cell membrane content of linoleic acid was 13% lower (P < .0001); arachidonic acid was 3.6% higher (P < .001); the trans isomer of oleic acid was 13.3% higher (P < .0001); and the trans-trans isomer of linoleic acid was 13.3% higher (P = .003). In multivariable analyses, a 1-SD decrease in linoleic acid was associated with >3 times the odds for being a case (odds ratio [OR] 3.23, 95% confidence interval [CI] 2.63-4.17). The relationship of arachidonic acid to ACS was U shaped; compared to the first quartile of arachidonic acid, the ORs for case status in the second, third, and fourth quartiles were 0.73 (95% CI 0.47-1.13), 0.65 (95% CI 0.41-1.04), and 2.32 (95% CI 1.39-3.90), respectively. The OR for a 1-SD increase in trans oleic acid was 1.24 (95% CI 1.06-1.45), and for trans-trans linoleic acid, 1.1 (95% CI 0.93-1.30). All associations were independent of membrane omega-3 FA content.. High blood levels of linoleic acid but low levels of trans oleic acid are inversely associated with ACS. The relationship of arachidonic acid to ACS appears more complex.

Topics: Acute Coronary Syndrome; Aged; Arachidonic Acid; Austria; Biomarkers; Case-Control Studies; Cholesterol; Erythrocyte Membrane; Fatty Acids, Omega-6; Female; Humans; Linoleic Acid; Male; Middle Aged; Myocardial Infarction; Oleic Acid; Reference Values; Risk Factors; Trans Fatty Acids; Triglycerides

Topics: Adult; Aged; Aged, 80 and over; alpha-Linolenic Acid; Animals; Coronary Disease; Death, Sudden, Cardiac; Denmark; Diet; Dietary Supplements; Fatty Acids; Fatty Acids, Omega-3; Fatty Acids, Omega-6; Female; Fish Oils; Fishes; Greenland; Health Surveys; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Japan; Linoleic Acid; Male; Middle Aged; Myocardial Infarction; Nurses; United States

Delta(6)-Desaturase (FADS2) is the rate-limiting step in the polyunsaturated fatty acid (PUFA) biosynthetic pathway.. The aim was to test whether the common deletion [T/-] in the promoter of FADS2 affects the PUFA biosynthetic pathway and consequently modifies the effect of alpha-linolenic acid (ALA) on myocardial infarction (MI).. Case subjects (n =1694) with a first nonfatal acute MI were matched by age, sex, and area of residence to 1694 population-based control subjects in Costa Rica. PUFAs were quantified by gas-liquid chromatography from plasma and adipose tissue samples. Least-squares means from generalized linear models and odds ratios (ORs) and 95% CIs from multiple conditional logistic regression models were estimated.. The prevalence of the variant T/- allele was 48%. Eicosapentaenoic acid, gamma-linolenic acid, and arachidonic acid decreased in adipose tissue and plasma with increasing number of copies of the variant allele with a monotonic trend (P < 0.05 for all). Fasting plasma triacylglycerols by genotype were 2.08 mmol/L for TT, 2.16 mmol/L for T-, and 2.26 mmol/L for - - [ie, homozygous for the variant (deletion) allele] (P = 0.03). The FADS2 deletion was not associated with MI and did not significantly modify the association between adipose tissue ALA and the risk of MI.. The FADS2 deletion may prevent the conversion of ALA into very-long-chain PUFAs. However, this metabolic effect is not translated into an attenuated risk between ALA and MI among carriers of the variant. It is possible that, at current intakes of ALA, any potential defect in the transcription of the gene is masked by the availability of substrate. Further research in populations deficient in ALA intake is warranted.

Topics: Aged; alpha-Linolenic Acid; Costa Rica; Fatty Acid Desaturases; Female; Gene Deletion; Gene Expression Regulation, Enzymologic; Genetic Predisposition to Disease; Humans; Linoleic Acid; Male; Middle Aged; Myocardial Infarction; Polymorphism, Genetic; Promoter Regions, Genetic; Risk Factors; Stearoyl-CoA Desaturase

There is a multitude of data showing that coronary heart disease is affected by the quality of dietary fat. The fatty acid composition of serum lipids has been shown to reflect that of the diet. It is likely that, after myocardial infarction, both the health-care professionals and the patients themselves pay more attention to dietary guidelines. In order to assess the correctness of this assumption, we compared the composition of serum fatty acids in 40 male subjects with a history of myocardial infarction (MI) with that of 40 age-matched controls, both from the FINRISK study. The percentage composition of fatty acids of total serum lipids was analysed by gas chromatography. In comparison with the control group, the MI group had higher body mass index (BMI), a higher prevalence of diabetes, higher level of serum triglycerides and a lower level of serum high-density lipoprotein (HDL) cholesterol, all indicators of the metabolic syndrome. The MI group had higher proportions of serum palmitic (16:0) and oleic acids (18:1), and a lower proportion of linoleic (18:2 n-6) acid than the control group. The metabolic syndrome is accompanied by an elevated level of serum insulin, which is known to enhance the synthesis of saturated and monounsaturated fatty acids, such as 16:0 and 18:1, and to stimulate the activity delta-6 desaturase, decreasing the concentration of linoleic acid. Our results suggest that the observed serum fatty acid composition in subjects with coronary heart disease is dependent on metabolic factors in addition to dietary fatty acid composition.

Topics: Aged; Body Mass Index; Cholesterol, HDL; Cross-Sectional Studies; Diabetes Mellitus, Type 2; Dietary Fats; Fatty Acids; Finland; Humans; Linoleic Acid; Male; Metabolic Syndrome; Middle Aged; Myocardial Infarction; Oleic Acid; Palmitic Acid; Triglycerides

Palm oil and soybean oil are the 2 most widely used cooking oils in the world. Palm oil is consumed mainly in developing countries, where morbidity and mortality due to cardiovascular disease (CVD) are on the rise. Although claims about adverse or protective effects of these oils are commonly made, there are no epidemiologic studies assessing the association between these oils and cardiovascular disease endpoints. We examined whether consumption of palm oil relative to soybean oil and other unsaturated oils (predominantly sunflower) is associated with myocardial infarction (MI) in Costa Rica. The cases (n = 2111) were survivors of a first acute MI and were matched to randomly selected population controls (n = 2111). Dietary intake was assessed with a validated semiquantitative FFQ. Adipose tissue profiles of essential fatty acids were assessed to validate cooking oil intake and found to be consistent with self-reported major oils used for cooking. The data were analyzed using conditional logistic regression. Palm oil users were more likely to have an MI than users of soybean oil [odds ratio (OR) = 1.33; 95% CI: 1.08-1.63] or other cooking oils (OR = 1.23; CI: 0.99-1.52), but they did not differ from users of soybean oil with a high trans-fatty acid content (OR = 1.14; CI: 0.84-1.56). These data suggest that as currently used in Costa Rica, and most likely in many other developing countries, the replacement of palm oil with a polyunsaturated nonhydrogenated vegetable oil would reduce the risk of MI.

Topics: Adipose Tissue; Aged; Alcohol Drinking; alpha-Linolenic Acid; Cooking; Costa Rica; Developing Countries; Diet Records; Dietary Fats, Unsaturated; Fatty Acids, Essential; Female; Folic Acid; Humans; Linoleic Acid; Male; Middle Aged; Myocardial Infarction; Palm Oil; Plant Oils; Risk Factors; Smoking; Soybean Oil; Vitamin B 6

Arachidonic acid (AA), a precursor of prothrombotic eicosanoids, is potentially atherogenic, but epidemiologic data are scarce. We evaluated the hypothesis that increased AA in adipose tissue is associated with increased risk of nonfatal acute myocardial infarction (MI), and if so, whether this association is related to dietary or adipose tissue linoleic acid. We studied the association between AA and MI in 466 cases of a first nonfatal acute MI, matched on age, gender, and residence to 466 population controls. Fatty acids (FA) were assessed by GC in adipose tissue samples collected from all subjects. Odds ratios (OR) and 95% CI were calculated from multivariate conditional logistic regression models. Subjects in the highest quintile of adipose tissue AA (0.64% of total FA) had a higher risk of nonfatal acute MI than those in the lowest quintile (0.29% of total FA), after adjusting for potential confounders including (n-3) and trans FAs (OR = 1.94, 95% CI: 1.07, 3.53, P for trend = 0.026). Adipose tissue AA was not correlated with dietary AA (r = 0.07), linoleic acid (r = 0.04), or other dietary (n-6) FAs, or with adipose tissue linoleic acid (r = -0.07). These data suggest that the association between MI and adipose tissue AA is not related to dietary intake of (n-6) FAs including linoleic acid. Better understanding of the metabolic factors that increase AA in adipose tissue is urgently needed.

Topics: Adipose Tissue; Age Factors; Aged; Arachidonic Acid; Body Size; Body Weight; Chromatography, Gas; Costa Rica; Diabetes Mellitus; Diet; Dietary Fats, Unsaturated; Female; Humans; Hypertension; Linoleic Acid; Logistic Models; Male; Middle Aged; Myocardial Infarction; Odds Ratio; Risk Factors; Sex Factors

The Jewish population of Israel consumes a diet rich in n-6 polyunsaturated fatty acids (PUFAs), principally linoleic acid. The consequences of this diet for ischemic heart disease (IHD) remain unclear.. We assessed the association of adipose tissue n-6 fatty acids, which are derived entirely from the diet, with acute myocardial infarction (AMI).. A total of 180 cases and 492 IHD-free controls aged 25-64 were included in a population-based case-control study of Jerusalem residents hospitalized with a first AMI. Diet was assessed by the use of a food-frequency questionnaire and adipose tissue fatty acids by gas chromatography of biopsy samples taken from subcutaneous gluteal tissue. The data were analyzed by multivariate logistic regression.. Dietary PUFAs (: 10.1% of energy) correlated (r = 0.43, P < 0.001) with adipose tissue linoleic acid, which constituted 25.6% of storage fatty acids. High intakes of linoleic acid were not associated with excess risk of AMI (age- and sex-adjusted odds ratio for the third versus the first tertile: 0.96; 95% CI: 0.62, 1.48; NS). In contrast, arachidonic acid, the long chain n-6 derivative of linoleic acid, was positively associated with AMI (age- and sex-adjusted odds ratio: 2.12; 95% CI: 1.33, 3.36; P = 0.004). With multivariate adjustment, there was no evidence for an adverse association of linoleic acid with AMI, whereas the risk associated with arachidonic acid persisted, albeit attenuated.. A very high linoleic acid intake does not appear to confer increased risk of nonfatal AMI. Nonetheless, the increased risk associated with arachidonic acid, a finding that requires confirmation, tempers an inference that diets rich in n-6 fatty acids are safe vis-à-vis coronary health.

Topics: Adipose Tissue; Adult; Arachidonic Acid; Case-Control Studies; Dietary Fats, Unsaturated; Fatty Acids, Omega-6; Fatty Acids, Unsaturated; Female; Humans; Jews; Linoleic Acid; Logistic Models; Male; Middle Aged; Myocardial Infarction; Myocardial Ischemia

Lipid peroxidation is initiated by cell damage. After homogenisation of porcine heart tissue in aqueous solution we observed the same lipid peroxidation products as detected after heart infarction. We used this observation to study the influence of ebselen (2-phenyl-1,2-benzoisoselenazol-3-(2H)-one) on the generation of oxidatively derived monohydroxy fatty acids and alpha-hydroxyaldehydes, typical lipid peroxidation (LPO) products. Heart tissue was homogenised before and after enzyme destruction and with addition of ebselen. The obtained LPO products were analysed by GC/MS after appropriate derivatisation and quantified by using internal standards. The amount of monohydroxy fatty acids and alpha-hydroxyaldehydes increased considerably in the porcine heart homogenates in which the enzymes were kept active. Addition of ebselen caused an additional significant increase of hydroxy fatty acids, while the increase of aldehydic compounds was less. These results confirm the glutathione peroxidase-like activity of ebselen but demonstrate also that it does not prevent lipid peroxidation.

Topics: Acetamides; Aldehydes; Animals; Antioxidants; Azoles; Cell Extracts; Fatty Acids; Fluoroacetates; Gas Chromatography-Mass Spectrometry; Isoindoles; Linoleic Acid; Linoleic Acids; Linoleic Acids, Conjugated; Lipid Peroxidation; Lipid Peroxides; Molecular Structure; Myocardial Infarction; Myocardium; Organoselenium Compounds; Plasmalogens; Swine; Trifluoroacetic Acid; Trimethylsilyl Compounds

The effects of dietary supplementation with fish on plasma fatty acid levels were studied in 20 coronary heart disease patients who had suffered acute myocardial infarction. The study was divided into three periods: hospital admission, after 8 weeks on a heart-healthy diet designed for patients with ischemic heart disease, and after 4 weeks on an n-3 fatty acid-supplemented diet in which red meat was replaced with lean and fatty fish. At the end of each period, the subjects responded to a 48-hour recall questionnaire, so that we could assess their compliance with the diet, and blood samples were collected for the determination of plasma fatty acids. Stearic fatty acid was significantly decreased after the fish diet. n-7 and n-9 fatty acids showed no significant changes throughout the study. At the end of the 4-week period when the fish diet was consumed, linoleic acid and its long-chain derivative docosapentaenoic acid (22:5 n-6) were significantly increased. The most notable changes in n-3 series fatty acids at the end of the third period were the significant decrease in linolenic acid and the significant increase in its long-chain derivatives eicosapentaenoic (20:5 n-3) and docosahexaneoic acid (22:6 n-3). These changes in plasma fatty acid levels may have beneficial effects on coronary heart disease.

Topics: Adult; alpha-Linolenic Acid; Coronary Disease; Dietary Fats, Unsaturated; Docosahexaenoic Acids; Eicosapentaenoic Acid; Fatty Acids; Fatty Acids, Omega-3; Fatty Acids, Omega-6; Fatty Acids, Unsaturated; Fish Oils; Humans; Linoleic Acid; Linoleic Acids; Male; Middle Aged; Myocardial Infarction; Oleic Acid; Oleic Acids

Free-radical generation after successful thrombolysis in acute myocardial infarction may jeopardize ischaemic but viable myocardium, thus limiting the optimal benefits of reperfusion.. Circulating free-radical activity was assessed in 25 consecutive patients with acute myocardial infarction. Those who successfully reperfused (Group A) were compared with those who did not (Group B). We also compared patients who had or had not developed Q waves and patients with and without previous angina or myocardial infarction. All patients presented within 6 h of the onset of chest pain and received standard intravenous streptokinase therapy. Free-radical activity in serial serum samples collected over 72 h was measured using the percentage molar ratio (PMR) of the concentrations of 9,11-linoleic acid to 9,12-linoleic acid, and malonaldehyde concentration.. Throughout the study period Group A (n = 11) showed significantly greater change in serum PMR and malonaldehyde levels compared with Group B (n = 14) (P < 0.01). PMR differences between the two groups were most pronounced at 3 and 12 h (P < 0.001). Patients with non-Q-wave myocardial infarction (n = 5) showed significantly greater changes in serum PMR and malonaldehyde levels (P < 0.01) compared with those with Q-wave infarction (n = 20). A history of previous infarction or angina had no apparent effects on the changes in serum free-radical activity.. Successful early reperfusion and non-Q-wave myocardial infarction are both associated with a significantly greater increase in the levels of markers of serum free-radical activity immediately after infarction. The results support present concepts of free-radical-mediated reperfusion injury. Use of these assays may identify those patients who may be at risk from free-radical-mediated reperfusion injury.

Topics: Aged; Biomarkers; Female; Free Radicals; Humans; Linoleic Acid; Linoleic Acids; Linoleic Acids, Conjugated; Male; Malondialdehyde; Middle Aged; Myocardial Infarction; Myocardial Reperfusion Injury; Thrombolytic Therapy; Treatment Outcome

Cardioprotective drugs are agents that prevent or moderate harmful consequences of impaired cardiac energetics, such as sudden coronary death (SCD) due to early post-occlusion ventricular fibrillation (EPVF), development of incapacitating myocardial necrosis. Cardioprotection may be due to anti-ischaemic action, correcting the imbalance between vascular supply and myocardial demand for blood, but also to cytoprotective effect, preserving cellular integrity in the presence of factors damaging structure and function of the cardiac cell membrane such as ischaemia, ionic imbalance and that of pH, etc. Neither anti-ischaemic nor cytoprotective effect alone, or in combination, are sufficient to warrant full cardioprotection, i.e. both prevention of SCD and limitation of infarct size. Thus the beta-blocker pindolol which is anti-ischaemic in its effect reducing myocardial O2 demand and protects from SCD and EVFP, failed to limit infarct size. Even interventions of a mainly cytoprotective type of action protecting from SCD and EPVF, such as the linoleic acid-rich diet, or lidocaine, were unable to limit infarct size, 7-oxoPGI2 (anti-ischaemic and cytoprotective) failed to protect from SCD, VF and did not limit infarct size. On the other hand the nonsteroidal anti-inflammatory drugs which, like salicylates or sulfinpyrazon, reduce myocardial O2 demand and protect from post-occlusion SCD and EPVF, effectively limiting infarct size.

Topics: Animals; Arrhythmias, Cardiac; Coronary Disease; Death, Sudden; Dietary Fats; Epoprostenol; Humans; Lidocaine; Linoleic Acid; Linoleic Acids; Myocardial Infarction; Pindolol

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.

Topics: Cardiovascular Diseases; Czechoslovakia; Dietary Fats; Energy Intake; Fatty Acids; Humans; Hyperlipoproteinemias; Linoleic Acid; Linoleic Acids; Male; Middle Aged; Myocardial Infarction; Myocardium; Prognosis

Topics: Fatty Acids; Humans; Linoleic Acid; Linoleic Acids; Lipids; Male; Middle Aged; Myocardial Infarction

Topics: Dietary Fats; Humans; Linoleic Acid; Linoleic Acids; Myocardial Infarction

Topics: Carbon Isotopes; Fatty Acids; Glycerides; Heart Diseases; Hyperlipidemias; Hypertriglyceridemia; Linoleic Acid; Lipid Metabolism; Lipids; Lipoproteins; Myocardial Infarction; Palmitates; Palmitic Acid; Tritium

Topics: Angina Pectoris; Blood Coagulation; Blood Coagulation Tests; Cholesterol; Diabetes Mellitus; Dietary Fats; Geriatrics; Humans; Linoleic Acid; Lipids; Myocardial Infarction; Palmitic Acid; Pharmacology; Stearic Acids; Thromboplastin; Triolein

Topics: Arteriosclerosis; Dietary Fats; Erythrocytes; Fatty Acids; Linoleic Acid; Lipids; Myocardial Infarction; Phospholipids; Statistics as Topic

Topics: Aortic Valve Stenosis; Arteriosclerosis; Bronchitis; Cholelithiasis; Diabetes Mellitus; Fatty Acids; Geriatrics; Hypertension; Injections, Intravenous; Kidney Function Tests; Linoleic Acid; Lung Diseases; Myocardial Infarction; Neurocirculatory Asthenia; Oleic Acid; Pharmacology; Phosphatidylcholines; Phospholipids; Pleurisy