Posts Tagged ‘role of EPA’

Stroke Prevention and Omega3 pharmaceutical grade fish oil EPA

Sunday, April 29th, 2012

Stroke Prevention and Omega3 pharmaceutical grade fish oil EPA

In a study based on a hypercholesterolemic patient population in Japan, subjects achieved secondary prevention of stroke with EPA.
In Japanese hypercholesterolemic patients with a history of stroke, EPA supplementation reduced the risk of stroke recurrence by 20%.
Further studies must be conducted with EPA to further understand potential benefits of EPA in stroke prevention.

The long-chain omega-3 fatty acideicosapentaenoic acid 20:5n-3 has been investigated for its role in preventing stroke recurrence. Specifically, the effects of EPA on stroke incidence were investigated as part of a large Japanese study known as the JELIS trial (Japan EPA Lipid Intervention Study). Conducted over a 5-year period, the JELIS trial examined the preventive effect of long-term supplementation with 1800 mg/day EPA on major coronary events and stroke in hypercholesterolemic patients in Japan
This large trial included over 18,000 individuals (15,000 without existing coronary artery disease and 3,645 with existing coronary artery disease), all between the ages of 40 and 75. All study participants were placed on statin therapy and then randomized in an open-label, endpoint-blinded manner to either an EPA 1800 mg/day group or a control group. The primary endpoint was any major cardiovascular event (sudden death, fatal or non-fatal myocardial infarction, unstable angina, angioplasty, or coronary artery bypass surgery). After a mean follow-up of 4.6 years, it was determined that EPA significantly suppressed the incidence of coronary events

A subanalysis of the JELIS trial was conducted with respect to stroke incidence, to determine whether EPA supplementation reduced the recurrence of stroke . The subanalysis examined the effects of EPA on stroke rates in 942 subjects with a history of stroke. Within this subgroup, stroke occurred in 48 (10.5%) of 457 subjects randomized to the no EPA group, and stroke occurred in 33 (6.8%) of 485 subjects randomized to the EPA group. Thus, EPA supplementation reduced the risk of stroke recurrence by 20%. The number needed to treat (i.e., the number of patients that a doctor would need to treat to prevent one stroke) was 27. These results indicate that 1800 mg/day EPA supplementation achieved secondary prevention of stroke in Japanese hypercholesterolemic patients. Furthermore, EPA supplementation did not raise the risk of subarachnoid hemorrhage or cerebral hemorrhage, indicating that EPA supplementation was safe vis-à-vis stroke risk

It should be noted that the JELIS trial population was exclusively Japanese, and this population exhibits a high background consumption of fish. The JELIS trial was the first to examine the particular effects of EPA on stroke recurrence. The results should inspire future studies to investigate the effects of EPA on stroke prevention in other populations.

Yokoyama M, Origasa H, Matsuzaki M, Matsuzawa Y, Saito Y, Ishikawa Y, Oikawa S, Sasaki J, Hishida H, Itakura H, Kita T, Kitabatake A, Nakaya N, Sakata T, Shimada K, Shirato K. Effects of eicosapentaenoic acid on major coronary events in hypercholesterolaemic patients (JELIS): a randomised open-label, blinded endpoint analysis. Lancet 2007;369:1090-1098.
Matsuzaki M, Yokoyama M, Saito Y, Origasa H, Ishikawa Y, Oikawa S, Sasaki J, Hishida H, Itakura H, Kita T, Kitabatake A, Nakaya N, Sakata T, Shimada K, Shirato K, Matsuzawa Y. Incremental effects of eicosapentaenoic acid on cardiovascular events in statin-treated patients with coronary artery disease. Circ J 2009;73:1283-1290.
Tanaka K, Ishikawa Y, Yokoyama M, Origasa H, Matsuzaki M, Saito Y, Matsuzawa Y, Sasaki J, Oikawa S, Hishida H, Itakura H, Kita T, Kitabatake A, Nakaya N, Sakata T, Shimada K, Shirato K. Reduction in the recurrence of stroke by eicosapentaenoic acid for hypercholesterolemic patients: subanalysis of the JELIS trial. Stroke 2008;39:2052-2058.
Harris WS. Substudies of the Japan EPA Lipid Intervention Study (JELIS). Curr Atheroscler Rep 2009;11:399-400.

The role of LDL-C and Type 2 Diabetes How Omega3 EPA fish oil reduces LDL-C

Sunday, April 29th, 2012

The role of LDL-C and Type 2 Diabetes

The U.K. Prospective Diabetes Study (UKPDS) established the importance of tight glycemic control in patients with diabetes. Yet in isolation, control of hyperglycemia is not sufficient to decrease the high burden of cardiovascular disease (CVD) in this population.Efforts to reduce cardiovascular morbidity and mortality in people with diabetes have therefore focused on overall or global risk factor management, including weight loss and increased physical activity, tight control of blood pressure and blood glucose, and intensive management of diabetic dyslipidemia. The typical lipid disorder in patients with diabetes, diabetic dyslipidemia, is characterized by elevated triglycerides, low levels of HDL cholesterol, and increased numbers of small, dense LDL particles.

Managing the high risk for cardiovascular morbidity and mortality in diabetic patients is a challenge for practicing clinicians. Reducing the burden of cardiovascular disease in diabetes should begin with assessment and treatment of elevated LDL cholesterol.The typical lipid disorder in patients with diabetes, diabetic dyslipidemia, is characterized by elevated triglycerides, low levels of HDL cholesterol, and increased numbers of small, dense LDL particles. The achievement of the intensive LDL cholesterol goals recommended by both the NCEP and the American Diabetes Association (ADA) has the potential to substantially improve long-term cardiovascular outcomes To this end, this review addresses three key issues related to lowering the risks associated with diabetic dyslipidemia: 1) the substantial CHD risk associated with relatively normal LDL cholesterol; 2) the value of lowering LDL cholesterol and normalizing atherogenic LDL particles in reducing cardiovascular risk; and 3) the role of intensive statin therapy in achieving aggressive LDL cholesterol goals.

Patients with diabetes frequently have lipid profiles that appear more benign than those of other high-risk people without diabetes. In general, LDL cholesterol levels in people with diabetes are not higher than those in people without diabetes who are matched for age, sex, and body weight. In fact, the most common LDL cholesterol level in diabetes is “borderline high” (130-159 mg/dl).12 Moreover, high LDL cholesterol levels (≥ 160 mg/dl) do not occur at higher-than-average rates in people with diabetes. Nonetheless, LDL cholesterol does not play less of a role in cardiovascular risk in people with type 2 diabetes. In fact, LDL cholesterol levels may understimate cardiovascular risk in diabetes. A large number of small, dense particles characterize the LDL fraction in diabetic individuals. These particles contain less cholesterol than normal-sized LDL particles, but they are exceptionally atherogenic.Thus, levels of LDL may appear deceptively “normal” in cholesterol measurements.

Small, dense LDL particles are considered more atherogenic than the larger, buoyant LDL particles because they are more readily oxidized and glycated, which make them more likely to invade the arterial wall.This can initiate atherosclerosis or lead to increased migration and apoptosis of vascular smooth muscle cells in existing atherosclerotic lesions. As a consequence, elevated or “normal” LDL cholesterol may be more pathogenic in people with diabetes.

Beyond the importance of even modest elevations in LDL cholesterol in people with diabetes, it also appears that LDL cholesterol interacts with risk factors of the metabolic syndrome to magnify the risk of CVD.The strong association between increased small, dense LDL particles and elevated triglycerides, for example, appears to be linked to the altered insulin sensitivity common in the metabolic syndrome and type 2 diabetes. Insulin resistance in skeletal muscle promotes the conversion of energy from ingested carbohydrate into increased hepatic triglyceride synthesis, which in turn generates large numbers of atherogenic triglyceride-rich lipoprotein particles, such as very-low-density lipoprotein (VLDL). As a further consequence, through the action of cholesteryl ester transfer protein, a significant amount of the triglyceride content of VLDL is exchanged for cholesterol in LDL particles, leading to the formation of triglyceride-enriched (and cholesterol-depleted) LDL These LDL particles are now primed to become smaller and denser through the actions of hepatic lipase-mediated triglyceride hydrolysis.Thus, adverse changes in LDL particles occur as triglyceride levels increase. Once triglyceride levels exceed 100 mg/dl, small, dense LDL particles predominate

Why eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)—both components of omega-3 fatty acids—have differential effects on LDL cholesterol.

Presenting the results of the laboratory study here at the National Lipid Association (NLA) 2011 Scientific Sessions, senior investigator Dr Preston Mason (Brigham and Women’s Hospital, Boston, MA) said that EPA is an inhibitor of lipid oxidation at normal and elevated cholesterol levels in the presence and absence of DHA, while DHA seems to have no real effect on lipid peroxidation. This trial was one of a number of studies that attempted to address the clinical question as to why LDL-cholesterol levels increase in patients treated with the triglyceride-lowering omega-3 fatty acids. In his trial, Mason et al compared the effects of EPA and DHA—alone or in combination with statins—on lipid peroxidation in polyunsaturated fatty-acid- and cholesterol-enriched vesicles.

“We know that EPA and DHA have different effects on LDL-cholesterol levels,”. “One of the things that affect LDL clearance is its oxidative state. Oxidized LDL is not cleared. One of the concepts is that EPA might preferentially prevent LDL oxidation, so even though it’s not affecting its synthesis, it would help its clearance.”

EPA inhibited lipid hydroperoxide (LOOH) formation by 42% and 54% in vesicles with normal and elevated cholesterol levels, respectively. DHA, on the other hand, inhibited LOOH by 28% in vesicles with elevated cholesterol levels only. The separate effects of EPA, DHA, and EPA/DHA were enhanced when used in combination with statin therapy, including atorvastatin, atorvastatin metabolite, simvastatin, or rosuvastatin. The most potent antioxidant capacity was observed with EPA and the active metabolite of atorvastatin.

In another analysis, Dr Terry Jacobson (Emory University School of Medicine, Atlanta, GA) and colleagues reviewed 21 clinical trials that systematically evaluated the effects of EPA and DHA as monotherapy on LDL-cholesterol, HDL-cholesterol, triglyceride, and non-HDL-cholesterol levels.

In studies that directly compared DHA and EPA, mean placebo-corrected triglyceride levels decreased by 22.4% and 15.6%, respectively. In head-to-head comparisons, DHA increased LDL cholesterol by 2.6% whereas EPA decreased LDL cholesterol by 0.7%. In trials comparing each agent alone, 10 of the 14 monotherapy trials with DHA showed increases in LDL cholesterol ranging from 5.4% to 16.0% vs control, while none of the EPA trials showed any increase. The changes in LDL-cholesterol levels significantly correlated with baseline triglyceride levels for DHA-treated patients, but this was not observed for patients treated with EPA, the group reported.

Speaking with heartwire, Dr William Harris (University of South Dakota, Sioux Falls), who was not involved in the research, said the issue is clinically important because numerous studies have shown that long-chain omega-3 fatty acids lower triglycerides, but randomized, clinical trials with compounds containing EPA and DHA have also shown increases in LDL-cholesterol levels. Lovaza / Omacor (omega-3 fatty acid ethyl esters, GlaxoSmithKline) is currently approved for the treatment of elevated triglyceride levels, but its use often results in an increase in LDL cholesterol. Harris noted that other drugs, including fibrates, have the potential to increase LDL cholesterol..

Omega 3 EPA reduces LDL cholesterol levels –

New clinical study results presented at the American Heart Association Scientific Sessions show that the long-chain omega-3 fatty acid EPA (eicosapentaenoic acid), helped significantly reduce small dense LDL (bad) cholesterol levels.

“This study suggests that supplementation with the omega-3 fatty acid EPA may present unique benefits for cardiovascular health,” said Sujata K. Bhatia, M.D., Ph.D., research associate with DuPont. “EPA was shown to have advantageous effects on several biomarkers, including LDL cholesterol, small dense LDL, and lp-PLA2.”

EPA is a long-chain fatty acid that is found primarily in cold water, fatty fish like sardines anchovies mackerel as well as some omega-3 fatty acid such as TakeOmega3 which has 750 mg EPA per capsule and is the highest grade omega 3 available in UK . A growing body of evidence suggests that EPA is the long-chain omega-3 that supports heart health.

The study, conducted by Cardiovascular Research Associates and sponsored by DuPont, was conducted among 110 healthy individuals comparing the effects of EPA supplements to DHA (docosahexaenoic acid) supplements on cardiovascular health. The participants were placed into four study groups and examined over a six week period. During that time, each group was monitored while taking: EPA 600 mg per day; EPA 1,800 mg per day; DHA 600 mg per day; and an olive oil placebo.

The study found that in the 1,800mg EPA group, there were significant reductions of 7 percent for small dense low density lipoprotein (LDL) cholesterol, and 6 percent for lipoprotein-associated phospholipase A2 (lp-PLA2). lp-PLA2 is an enzyme involved in vascular inflammation.

In contrast, the 600mg DHA group showed a significant increase in total small dense LDL cholesterol in both the fasting and fed state of 14.2 percent and 16.3 percent respectively.

The study results will be featured during the American Heart Association Conference poster session in Chicago

Omacor contains 375mg DHA just two capsules exceeds the 600mg DHA level that shows an increase in LDL C – on a 4 capsule per dose dose that would deliver 1500 mg of DHA which is more than double the dose that showed a 14.2 % and 16.3% increase in small dense LDL

Omega-3 fish oil essential fatty acids Significantly Improves The Endothelial Function

Thursday, April 5th, 2012

Omega-3 fish oil essential fatty acids Significantly Improves The Endothelial Function

Wang Q, Liang X, Wang L, et al. Effect of omega-3 fatty acids supplementation on endothelial function: A meta-analysis of randomized controlled trials. Atherosclerosis. 2012 Apr;221(2):536-43.

Inverse association was reported between omega-3 fatty acids (FAs) supplementation and the risk of cardiovascular disease. Identifying the effect of omega-3 FAs on endothelial function may contribute to explain the association. We conducted a meta-analysis to assess the effect of omega-3 FAs supplementation on endothelial function, as measured by flow-mediated dilation (FMD) and endothelium-independent vasodilation (EIV).

Randomized placebo-controlled trials (RCTs) were identified from the databases of PubMed, EMBASE and Cochrane library by two investigators and the pooled effects were measured by weighted mean difference (WMD), together with 95% confidence intervals (CIs). Subgroup and meta-regression analyses were used to explore the source of between-study heterogeneity.

Totally 16 eligible studies involving 901 participants were finally included in meta-analysis. Compared with placebo, omega-3 FAs supplementation significantly increased FMD by 2.30% (95% CI: 0.89-3.72%, P=0.001), at a dose ranging from 0.45 to 4.5g/d over a median of 56days. Subgroup analyses suggested that the effect of omega-3 FAs on FMD might be modified by the health status of the participants or the dose of supplementation. Sensitivity analyses indicated that the protective effect of omega-3 on endothelial function was robust. No significant change in EIV was observed after omega-3 FAs supplementation (WMD: 0.57%; 95% CI: -0.88 to 2.01%; P=0.442).
he loss of proper endothelial function, is a hallmark for vascular diseases, and is often regarded as a key early event in the development of atherosclerosis. Impaired endothelial function, causing hypertension and thrombosis, is often seen in patients with coronary artery disease, diabetes mellitus, hypertension, hypercholesterolemia, as well as in smokers.
Supplementation of omega-3 fatty acids significantly improves the endothelial function without affecting endothelium-independent dilation

Omega-3 fish oil is Linked To Decreased Inflammation And Decreased Fatigue in Breast Cancer

Saturday, March 17th, 2012

Omega-3 fish oil is Linked To Decreased Inflammation And Decreased Fatigue in Breast Cancer – Omega 3 active ingredient EPA is the most potent natural anti inflammatory
Alfano CM, Imayama I, Neuhouser ML, et al. Fatigue, Inflammation, and ω-3 and ω-6 Fatty Acid Intake Among Breast Cancer Survivors. J Clin Oncol. 2012 Mar 12.
PURPOSE: Evidence suggests that inflammation may drive fatigue in cancer survivors. Research in healthy populations has shown reduced inflammation with higher dietary intake of Omega 3 ω-3 polyunsaturated fatty acids (PUFAs), which could potentially reduce fatigue. This study investigated fatigue, inflammation, and intake of Omega 3 ω-3 and Omega 6 ω-6 PUFAs among breast cancer survivors.

METHODS: Six hundred thirty-three survivors (mean age, 56 years; stage I to IIIA) participating in the Health, Eating, Activity, and Lifestyle Study completed a food frequency/dietary supplement questionnaire and provided a blood sample assayed for C-reactive protein (CRP) and serum amyloid A (30 months after diagnosis) and completed the Piper Fatigue Scale and Short Form-36 (SF-36) vitality scale (39 months after diagnosis). Analysis of covariance and logistic regression models tested relationships between inflammation and fatigue, inflammation and Omega3 ω-3 and Omega 3 ω-6 PUFA intake, and PUFA intake and fatigue, controlling for three incremental levels of confounders. Fatigue was analyzed continuously (Piper scales) and dichotomously (SF-36 vitality ≤ 50).

Results: Behavioral (P = .003) and sensory (P = .001) fatigue scale scores were higher by increasing CRP tertile; relationships were attenuated after adjustment for medication use and comorbidity. Survivors with high CRP had 1.8 times greater odds of fatigue after full adjustment (P < .05). Higher intake of ω-6 relative to ω-3 PUFAs was associated with greater CRP (P = .01 after full adjustment) and greater odds of fatigue (odds ratio, 2.6 for the highest v lowest intake; P < .05).

CONCLUSION: Results link higher intake of Omega3 ω-3 PUFAs, decreased inflammation, and decreased physical aspects of fatigue. Future studies should test whether Omega3 ω-3 supplementation may reduce fatigue among significantly fatigued breast cancer survivors.

Omega3 highest concentration is found in takeomega3 which is high in the active omega3 EPA - the most potent natural anti inflammatory . TakeOmega3 is a unique pharmaceutical grade formulation manufactured in MHRA facilities in the UK . It is an 85% concentration with each capsule containing 750mg EPA and 50mg DHA.

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Made in the UK - Take Omega 3 Suspendisse lacinia ultricies justo, at ultricies nisi tempus ac. Cras sed vehicula metus. Phasellus...