Quantitative effects on cardiovascular risk factors and coronary heart disease risk of replacing partially hydrogenated vegetable oils with other fats and oils. Kris-Etherton P. The debate about n-6 polyunsaturated fatty acid recommendatons for cardiovascular health. Han S. Effect of hydrogenated and saturated, relative to polyunsaturated, fat on immune and inflammatory responses of adults with moderate hypercholesterolemia. Lipid Res. Twentieth-century trends in essential fatty acid intakes and the predicted omega-3 index: evidence versus estimates. Gebauer S. Craig W. Position of the American Dietetic Association: vegetarian diets.
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Aarsetoey H. Myerburg R. Frequency of sudden cardiac death and profiles of risk. Wilhelm M. Red blood cell omega-3 fatty acids and the risk of ventricular arrhythmias in patients with heart failure. Heart J. Sudden cardiac death caused by coronary heart disease. Streppel M. Long-term fish consumption and n-3 fatty acid intake in relation to sudden coronary heart disease death: the Zutphen study. Low levels of cellular omega-3 increase the risk of ventricular fibrillation during the acute ischaemic phase of a myocardial infarction. Low levels of the omega-3 index are associated with sudden cardiac arrest and remain stable in survivors in the subacute phase.
Von Schacky C. Omega-3 fatty acids vs. Cell Mol. Huikuri H. Sudden death due to cardiac arrhythmias. Omega-3 fatty acids: anti-arrhythmic, pro-arrhythmic or both? Raitt M.
Fish oil supplementation and risk of ventricular tachycardia and ventricular fibrillation in patients with implantable defibrillators: a randomized controlled trial. Brouwer I. Effect of fish oil on ventricular tachyarrhythmia in three studies in patients with implantable cardioverter defibrillators.
Altered myocardial fatty acid and glucose metabolism in idiopathic dilated cardiomyopathy. Herrero P. Increased myocardial fatty acid metabolism in patients with type 1 diabetes mellitus. Rijzewijk L. Altered myocardial substrate metabolism and decreased diastolic function in nonischemic human diabetic cardiomyopathy: studies with cardiac positron emission tomography and magnetic resonance imaging.
Goldberg I. Lipid metabolism and toxicity in the heart. Cell Metab. Jump D. N-3 polyunsaturated fatty acid regulation of hepatic gene transcription. Park W. An alternate pathway to long chain polyunsaturates: the FADS2 gene product Delta8-desaturates n-6 and n Gregory M. Elongase reactions as control points in long-chain polyunsaturated fatty acid synthesis. Stroud C. Disruption of FADS2 gene in mice impairs male reproduction and causes dermal and intestinal ulceration.
Soraphen A, a inhibitor of acetyl CoA carboxylase activity, interferes with fatty acid elongation. Fan Y. Characterization of an arachidonic acid-deficient Fads1 knockout mouse model. Huang Y. Eicosadienoic acid differentially modulates production of inflammatory modulators in murine macrophages. Jakobsson A. Fatty acid elongases in mammals: their regulation and role in metabolism. Guillou H. The key roles of elongases and desaturases in mammalian fatty acid metabolism: insights from transgenic mice.
Wang Y. Tissue-specific, nutritional, and developmental regulation of rat fatty acid elongases. Regulation of hepatic fatty acid elongase and desaturase expression in diabetes and obesity. Tripathy S. Igarashi M. Rat heart cannot synthesize docosahexaenoic acid from circulating alpha-linolenic acid because it lacks elongase Rapoport S. Quantitative contributions of diet and liver synthesis to docosahexaenoic acid homeostasis. Prostaglandins Leukot. Fatty Acids.
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Pawar A. Unsaturated fatty acid regulation of peroxisome proliferator-activated receptor alpha activity in rat primary hepatocytes. Ryan A. The hypolipidemic effect of an ethyl ester of algal-docosahexaenoic acid in rats fed a high-fructose diet. Brossard N. Retroconversion and metabolism of [13C] ,n-3 triacylglycerols. Plourde M. Plasma incorporation, apparent retroconversion and beta-oxidation of 13C-docosahexaenoic acid in the elderly. Fatty acid regulation of hepatic gene expression. Gao F.
The Warning on Saturated Fat: From Defective Experiments to Defective Guidelines
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Associations between estimated fatty acid desaturase activities in serum lipids and adipose tissue in humans: links to obesity and insulin resistance. Lipids Health Dis. Kawashima A. Plasma fatty acid composition, estimated desaturase activities and intakes of energy and nutrient in Japanese men with abdominal obesity or metabolic syndrome. Pachikian B. Hepatic n-3 polyunsaturated fatty acid depletion promotes steatosis and insulin resistance in mice: genomic analysis of cellular targets. Glaser C. Genetic variation in polyunsaturated fatty acid metabolism and its potential relevance for human development and health.
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Bokor S. Single nucleotide polymorphisms in the FADS gene cluster are associated with delta-5 and delta-6 desaturase activities estimated by serum fatty acid ratios.
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Mathias R. FADS genetic variants and omega-6 polyunsaturated fatty acid metabolism in a homogeneous island population. Lemaitre R.
Genetic loci associated with plasma phospholipid n-3 fatty acids: a meta-analysis of genome-wide association studies from the CHARGE Consortium. PLoS Genet. Ohno Y. Tanaka T. Aslibekyan S. Genetic variation in fatty acid elongases is not associated with intermediated cardiovascular phenotypes or myocardial infarction. Stoffel W. Delta-6 desaturase FADS2 deficiency unveils the role of omega-3 and omega-6 polyunsaturated fatty acids. EMBO J.
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The role of G-protein-coupled receptors in mediating the effect of fatty acids on inflammation and insulin sensitivity. Saltiel A. Fishing out a sensor for anti-inflammatory oils. Wada M. Enzymes and receptors of prostaglandin pathways with arachidonic acid-derived versus eicosapentaenoic acid-derived substrates and products. Smith W. Nutritionally essential fatty acids and biologically indispensable cyclooxygenases.
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Arnold C. Arachidonic acid-metabolizing cytochrome P enzymes are targets of omega-3 fatty acids. Cytochrome Pdependent metabolism of omega-6 and omega-3 long-chain polyunsaturated fatty acids. Falck J. Although we conducted a large number of statistical tests, the analyses for the main FA families were designed using a priori hypotheses. Despite not being in line with the putative biological effects of their metabolites, the AA and DGLA results are consistent with previous studies in different settings in the US and Europe. The results for odd chain FAs have some previous support, but will need confirmation in future studies.
We only measured the two most common trans-fatty acids n9trans, n9trans.
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Though we were unable to assess the transisomers associated with CHD in other studies  , at the very low concentrations in a range more typical of European populations  , there was little power to assess the trans-fatty acid—CHD relationship. We controlled for the major lifestyle and demographic factors related to CHD risk but cannot exclude residual confounding with other unknown factors.
We used only plasma FAs measured one point in time to characterise individuals. There is likely to be large intraindividual variation in FAs but such random measurement error is likely to attenuate any relationships, rather than produce spurious associations. Future studies examining the relationship between FAs and CHD need to consider heterogeneity in the biological and health effects of individual FAs as well as the overall FA profile and balance between FAs.
The ability to assess these associations in human populations has been constrained by the limitations of assessing dietary fat intake. Biochemical measures offer more objective and specific biomarkers, which may provide greater insight into exogenous dietary factors as well as endogenous metabolic processes which influence risk of chronic diseases. It is beyond the remit of the current study to quantify in absolute amounts the relationship between blood FA concentrations and dietary intake of foods and nutrients, It is not clear how far the associations reflect complex interactions between dietary fat intake per se and FA metabolism, which may have both genetic and other exogenous influences.
Nevertheless, the major sources of dietary n-6 PUFA, i. While dietary recommendations should focus on general patterns of food intake rather than individual nutrients  , recommendations still need to be based on knowledge of the biological roles of different nutrients and balance between different nutrients in foods.
Just as recommendations now acknowledge differences in health effects of different families of fats, so they should evolve to reflect increasingly discriminating understanding of individual FA metabolism, and their interactions. Early guidelines to prevent CHD recommended reductions in saturated fat but little consistency as to what might be substituted: other fats, protein, or carbohydrate.
Our results add to the accumulating evidence that substitution of saturated fat by n-6 polyunsaturated fat may have more CHD benefits  ,  , . Detailed description of the analytic methods for plasma phospholipid measurements. Odds ratio for plasma PFAs per approximate SD, PFA increase, adjusted for age, sex, BMI, smoking, alcohol intake, physical activity, plasma vitamin C, social class, education, diabetes, systolic blood pressure, total energy intake, total carbohydrate intake, total protein intake.
Enrolled patients: KTK. Abstract Background The lack of association found in several cohort studies between dietary saturated fat and coronary heart disease CHD risk has renewed debate over the link between dietary fats and CHD. Methods and Findings We assessed the relationship between plasma phospholipid fatty acid PFA concentration and incident CHD using a nested case control design within a prospective study EPIC-Norfolk of 25, individuals aged 40—79 years examined in — and followed up to Conclusions In this study, plasma concentrations of even chain saturated PFA were found to be positively and omega-6 polyunsaturated PFA inversely related to subsequent coronary heart disease risk.
Please see later in the article for the Editors' Summary. Editors' Summary Background Coronary heart disease CHD is a condition caused by a build-up of fatty deposits on the inner walls of the blood vessels that supply the heart, causing the affected person to experience pain, usually on exertion angina. Why Was This Study Done? What Did the Researchers Do and Find? What Do These Findings Mean?
Information about the EPIC-Norfolk study is available The American Heart Foundation provides patient-friendly information about different dietary fats as does Medline The British Heart Foundation also provides patient-friendly information on heart conditions. Introduction Dietary fat intake has long been implicated in the aetiology of coronary heart disease CHD. Methods The European Prospective Investigation into Cancer EPIC -Norfolk is a prospective study of 25, men and women aged 40—79 years in Norfolk, UK similar in characteristics to UK general population samples, who participated in a baseline survey in — .
Selection of Cases and Controls From all the individuals with available measurement of plasma phospholipid FAs, we identified 2, individuals who had incident CHD and 4, control individuals alive and free of known cardiovascular disease during follow-up to Results Table 1 shows baseline characteristics of the 2, individuals with incident CHD fatal and 4, controls. Download: PPT. Table 1. Table 2. Baseline characteristics of participants by quartile of plasma saturated PFA concentration. Table 3.
The dietary fat–heart disease hypothesis: An ongoing debate Anaizi N - Ibnosina J Med Biomed Sci
Table 4. Table 5. Discussion There was no overall association between total plasma phospholipid FA concentration and CHD and only weak associations were observed for each family of FAs considered in isolation. Supporting Information. Text S1. Text S2. References 1. Eur J Clin Nutr S5— View Article Google Scholar 2.
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PLoS Med 7: e View Article Google Scholar 7. Skeaff CM, Miller J Dietary fat and coronary heart disease: summary of evidence from prospective cohort and randomised controlled trials. Ann Nutr Metab — View Article Google Scholar 8. Cantwell MM Assessment of individual fatty acid intake. Proc Nutr Soc — View Article Google Scholar 9.
Prog Lipid Res — View Article Google Scholar Lipids Health Dis 4: Wolk A, Furuheim M, Vessby B Fatty acid composition of adipose tissue and serum lipids are valid biological markers of dairy fat intake in men. J Nutr — Am J Epidemiol — Thanks for a well explained post. My take on this is, i think its way more complicated to understand what is the real culprit behind heart attack, as it is more evident that there is no single source. People just need to adjust to living healthy! To exercise, and eat health meals but more importantly healthy portion. If the degeneration of cholesterol or, more precisely, the lipoprotein carrying it is the culprit and not the cholesterol itself, would the reduction in the quantity of cholesterol be beneficial in preventing degeneration?
Would it not be better to address the underlying cause of the degeneration rather than focusing on the source of one of the components of the molecule that ultimately goes bad? But by adjusting it a little bit, most of it posted twice. But then both disappeared, a short time later. Hi Warren — thank you very much for your comments. We always have to manually approve comments, hence why yours did not appear straight away.
A recent systematic review of the medial literature shows that short stature is associated with increased risk of CHD. I eat little meat, but. I follow. Having worked as a cardiovascular nurse, i was always highly skeptical of the cholesterol theory. On a purely anecdotal level, i had greater suspicions about refined carbohydrates, sugars, and resulting inflammation than the consumption of saturated fats.
I have also been highly suspicious of chemically altered fats such as hydrogenated vegetable oils if for no other reason than their introduction and widespread use correlated well with increase in cardiovascular disease. I also had similar skepticism about aspirin therapy as a risk reduction strategy.
The default position is to give both patients and physicians something they can do or control to prevent what is, at least to this point, rather inevitable as we age. No doctor or patient wants to hear that their is little that can be done about complex disease processes. A little humility and an open mind that we could be wrong is far more helpful than medical dogma. Perhaps an example of my own personal bias, I thoroughly expected these articles to be riddled with inaccuracies; maybe they would even go so far as to claim a causal link with cancer.
Though by no means perfect, I was pleasantly surprised with the content of these pieces, ran by. Rich Thorley takes a closer look at the reporting of statistics in a recent story about the health benefits of coffee. What are the key steps in EBM? Who are S4BE? Cholesterol heart disease.
Twitter: sashalfrost View more posts from Sasha. Leave a Reply Cancel reply Your email address will not be published. Hedley Finger I have been reading lately that atherosclerosis is a disease of blood vessel inflammation, and that cholesterol is just an innocent bystander. July 6, at pm Reply to Hedley. Rob Seddon-Smith There is much to be said for your research.