Archive for April, 2012

Omega 3 EPA( Eicosapentaenoic Acid) protects against acid induced colitis

Monday, April 30th, 2012

Resolvin E1, an endogenous lipid mediator derived from omega-3 eicosapentaenoic acid, protects against 2,4,6-trinitrobenzene sulfonic acid-induced colitis.
Arita M, Yoshida M, Hong S, Tjonahen E, Glickman JN, Petasis NA, Blumberg RS, Serhan CN.
Source
Center for Experimental Therapeutics and Reperfusion Injury, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA 02115, USA.
Abstract
Resolvin E1 (RvE1; 5S,12R,18R-trihydroxyeicosapentaenoic acid) is an antiinflammatory lipid mediator derived from omega-3 fatty acid eicosapentaenoic acid (EPA). At the local site of inflammation, aspirin treatment enhances EPA conversion to 18R-oxygenated products, including RvE1, which carry potent antiinflammatory signals. Here, we obtained evidence for reduced leukocyte infiltration in a mouse peritonitis model, where the administration of EPA and aspirin initiated the generation of RvE1 in the exudates. Similar results were obtained with the administration of synthetic RvE1, which blocked leukocyte infiltration. RvE1 also protected against the development of 2,4,6-trinitrobenzene sulfonic acid-induced colitis. The beneficial effect was reflected by increased survival rates, sustained body weight, improvement of histologic scores, reduced serum anti-2,4,6-trinitrobenzene sulfonic acid IgG, decreased leukocyte infiltration, and proinflammatory gene expression, including IL-12 p40, TNF-alpha, and inducible nitric oxide synthase. Thus, the endogenous lipid mediator RvE1 counter-regulates leukocyte-mediated tissue injury and proinflammatory gene expression. These findings show an endogenous mechanism that may underlie the beneficial actions of omega-3 EPA and provide targeted approaches for the treatment of intestinal inflammation

Omega3 Fish oil may counteract procarcinogenic actions

Monday, April 30th, 2012

Omega-3 essential fatty acid Fish Oil Intake May Counteract Procarcinogenic Actions

Touvier M, Kesse-Guyot E, Andreeva VA, et al. Modulation of the association between plasma intercellular adhesion molecule-1 and cancer risk by n-3 PUFA intake: a nested case-control study. Am J Clin Nutr. 2012 Apr;95(4):944-50.

BACKGROUND:
Mechanistic data suggest that n-3 PUFAs and endothelial function may interact and play a role in carcinogenesis, but epidemiologic evidence is lacking.

OBJECTIVE:
Our objective was to investigate whether the prospective association between soluble intercellular adhesion molecule-1 (sICAM-1) and cancer risk is modulated by n-3 PUFA intake.

DESIGN:
A nested case-control study was designed to include all first-incident cancer cases diagnosed in the SUpplémentation en VItamines et Minéraux AntioXydants cohort between 1994 and 2007, with available dietary data from 24-h records (n = 408). Cases were matched with 1 or 2 randomly selected controls (n = 760). Conditional logistic regression was used to estimate ORs and 95% CIs for the association between prediagnostic plasma concentrations of sICAM-1 and cancer risk, stratified by n-3 PUFA intake. The interactions between sICAM-1 and n-3 PUFA intake were tested.

RESULTS:
An interaction was observed between sICAM-1 and n-3 PUFA intake, which was consistent across the studied cancer locations (P-interaction = 0.036 for overall, 0.038 for breast, and 0.020 for prostate cancer risk). sICAM-1 concentrations were positively associated with cancer risk among subjects with n-3 PUFA intakes below the median (multivariate OR(Tertile3vsTertile1): 2.8; 95% CI: 1.5, 5.2; P-trend = 0.001), whereas this association was not observed for subjects with n-3 PUFA intakes above the median (OR(Tertile3vsTertile1): 1.3; 95% CI: 0.8, 2.3; P-trend = 0.3).

CONCLUSION:
These findings suggest that n-3 PUFA intake may counteract the procarcinogenic actions of sICAM-1. This trial was registered at clinicaltrials.gov as NCT00272428

Association Between Rheumatoid Arthritis and Systemic Bone Loss Highlights the Importance of Omega-3 Anti-Inflammatory Diet

Monday, April 30th, 2012

Association Between Rheumatoid Arthritis and Systemic Bone Loss Highlights the Importance of Omega-3 Anti-Inflammatory Diet

A newly published study, in the Rheumatology International, finds a relation between an inflammatory agent, found in Rheumatoid Arthritis patients, and early bone loss. The study suggests repressing this inflammatory agent as a remedy for treatment. Nutri-Med Logic Corp, agreeing with this study, adds that while supplementation of nutrients such as calcium and vitamin D are highly important in combating osteoporosis but this study correctly identifies an under-looked but yet an important cause of bone loss: “Inflammation.”

Miami, FL (PRWEB) April 27, 2012

A newly published study states that an inflammatory agent “IL-6″ implicated in the manifestation of Rheumatoid Arthritis (RA) plays a key and fundamental role in bone loss in RA patients. Nutri-Med Logic Corp, agreeing with this study, adds that an uncontrolled inflammation not only results in bone loss in RA patients, but also remains a key cause of the osteoporosis in general population and thus more emphasis is needed for the incorporation of Omega-3 anti-inflammatory diet.

While calcium and vitamin D are taking the front stage, as the dietary intervention of choice to prevent and/or improve osteoporosis, but it is the inflammation that remains the main culprit, yet it has been the most under-looked cause of osteoporosis.

Calcium is a key component of the bone matrix. However, absorption of calcium is dependent on two key factors: Homeostasis of inflammation and availability of a group of other minerals, those being vitamin D, vitamin K, phosphate, baron, manganese and magnesium.

Even with adequate intake of calcium and its mineral group, osteoporosis is very likely if inflammation remains dysregulated.

This study correctly identifies an inflammatory agent “IL-6″, found in RA patients, and relates it to bone resorption in this group. However, excess production of IL-6 not only is the cause of bone loss in RA patients but also the key and fundamental player in the development and progression of osteoporosis.

IL-6 is an important biologic molecule that separates the work of bone-making cells and bone-removing cells. IL-6 activates the bone resident immune cells (macrophages) and converts them to osteoclasts, which are the bone-removing cells.

The genes that produce IL-6 share a binding site with another gene that produces the master switch of inflammation, that being NF-kB, whereas activation of one results in the activation of the other. (Proceeding of National Academy of Science, Vol. 90, pp. 10193- 10197, Nov. 1993.)

Moderation and/or inhibition of NF-kB is the key target of most, if not all, osteoporosis medication.

According to studies by the Department of Experimental Medicine and Oncology, University of Turin, Italy, NF-kB could also be moderated by means of a suitable dietary intake of Omega-3.

Omega-3 Adequate Intake (AI) recommendation, from the Food and Nutrition Board of The U.S. Institute of Medicine (IOM) stands at 1.1 to 1.6g/d (gram per day) for Women and Men, respectively, in order to prevent its deficiency and/or promote health. The IOM is the health arm of the National Academy of Sciences, which works outside of government to examine the US nutritional well-being, establishes the Adequate Intake (AI) of nutrients, as well as providing guidance about the application of nutrition and food sciences to improve human health.

Omega3 EPA accelerates ligament healing

Sunday, April 29th, 2012

Ligaments are tough bands of fibrous connective tissue (mainly collagen) that link two bones together at a joint. Injuries to ligaments are notoriously slow to heal. Researchers at Purdue University now report the results of an intriguing experiment which shows that eicosapentaenoic acid (EPA – the main component of fish tissue oils) materially speeds up the healing of “wounded” ligament cells in vitro. The experiment was carried out on three cultures of animal medial collateral ligament cells. The first culture was treated with arachidonic acid (an n-6 polyunsaturated fatty acid), the second with eicosapentaenoic acid (an n-3 polyunsaturated fatty acid), and the third served as a control.

After four days the cells were analyzed to determine their fatty acid profile. The AA (arachidonic acid) treated cells were found to have an n-6 to n-3 ratio of 24.3 while the EPA (eicosapentaenoic acid) treated cells had a ratio of 1.1. This indicates that the two fatty acids were well-absorbed and incorporated into the cells. Next a “wound” was introduced into the surface layers of the cell cultures by streaking a sterile pipette across them. The rate at which ligament cells grew back into the “wound” was measured over a 72-hour period and taken as an indication of wound healing speed. Both the AA and EPA treated cultures showed a higher degree of regrowth in the wound area than did the control. However, while AA decreased the synthesis of collagen by the ligament cells, EPA markedly increased it.

The researchers conclude that dietary supplementation with fish oils (n-3 polyunsaturated fatty acids) could be used to improve the healing of ligament injuries by enhancing the entry of new cells into the wound area and by speeding up collagen synthesis.

Source

Hankenson, Kurt D., et al. Omega-3 fatty acids enhance ligament fibroblast collagen formation in association with changes in interleukin-6 production. Proceedings of the Society for Experimental Biology and Medicine

Research shows that omega3 fish oil less than 80% concentrate are not effective at reducing triglyceride levels

Sunday, April 29th, 2012

t research has shown that lower concentrates omega 3 fish oil are not effective especially at reducing triglyceride levels

A study conducted in Europe showed the following that in order for omega3 to be effective in this area it required a concentration of at least 80% and above – none of the products by Nordic Naturals fall into this category or indeed any of those listed on the spreadsheet . The study concluded that “low concentration makes fish oil products impreactical for therapeutic use ”

The study looked at the Omega-3 uptake of three different Omega-3 concentrations:
62% Omega-3 (often sold as ‘Triple Strength’)
80% Omega-3
85% Omega-3
They did not test the regular ‘drug store grade’ fish oil (30% Omega-3) because it was ‘impractical’ to expect anyone to take 10 pills a day.

Every patient in the study took 5,100 mg (5.1 grams) of Omega-3 per day. However the big differentiate was the concentration levels

62% Did Not lower triglycerides

80% Did lower triglycerides

85% Did lower triglycerides

- there is an argument that omega3 at 62% Omega-3 is not pharmaceutical grade , however 80% to 85% are indeed

What was shown when they evaluated the results of the study was the following

A
There was a significant increase in blood EPA omega3 levels just after 14 days

B

The concentration levels of EPA were highest in the group taking the 85% concentration – the levels were lower in 62% and 80% group

C

The were no differences in the levels of DHA omega3 levels across the 3 groups

D

The most important factor was that the 62% omega3 concentrate did NOT lower triglycerides only the 80% and 85% omega3 fish oil did

RESULT: Even though everyone took the same amount of Omega-3, the chart below shows that 80% and 85% oils were better ‘absorbed.’

This is why it’s critical to take omega3 products such as TakeOmega3 that provide at least 80% Omega-3 concentrations.TakeOmega3 has 990mg omega3 and is an with 85% EPA /DHA concentration
It is very important that most fish oil supplements marketed as pharmaceutical grade or triple strength are only 60% omega 3 concentration

RESULT: Percent change in Triglycerides after taking 62%, 80% and 85% Omega-3 fish oil.

‘Triple Strength’ Fish Oil reduced triglycerides by less than 5% after two weeks. 80% and 85% Omega-3 oils reduced triglycerides by about 20%.
Since the FDA and other agencies does not regulate the terms like ‘pharmaceutical grade,’or ‘Triple Strength,’ anyone can call their product anything they want.However to gain CPP certification a product must fully comply with the conditions as stated by the MHRA – TakeOmega3 offers the highest concentration EPA of any formulation and is certificated by the MHRA

The reason the low concentrates dont work specifically with regards triglyceride reduction is very simple – yes its 62% omega3 but its also almost 40% or one-third non omega3 fats – whereas any oil that is 85% EPA and DHA such as TakeOmega3 will also be 90% in total omega3 as a result there is liitle if any other fatty acids. Omega-3 fats are a poor substrate for synthesis for triglycerides and Omega-3 also inhibit enzyme, acyl CoA:1,2-diacylglycerol acyltransferase due to the natural affinity Omega-3 has for this enzyme.

Harvard Medical School. Charles Serhan, a Harvard Medical School expert on Omega-3:
“The kind of benefits seen in most of the clinical trials with Omega-3 generally have involved much higher doses than you see recommended on supplement labels.”

Wall Street Journal. “Fish-Oil Doses Can Be Hard To Swallow,” David Stipp in Wall Street Journal Special Report, January 8, 2008:
“In trials aimed at lowering triglycerides, patients took three grams of Omega-3 per day. You would have to pop a daily dozen of the typical Omega-3 capsules on the market to get that.”

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.

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

Sunday, April 29th, 2012

resenting 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..

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 pharmaceutical grade fish oil EPA reduces LDL cholesterol levels

Sunday, April 29th, 2012

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

BENEFICIAL EFFECT OF EICOSAPENTAENOIC ACID ON ENDOTHELIAL FUNCTION IN OLD MYOCARDIAL INFARCTION PATIENTS UNDER ADEQUATE STATIN THERAPY

Sunday, April 29th, 2012

BENEFICIAL EFFECT OF EICOSAPENTAENOIC ACID ON ENDOTHELIAL FUNCTION IN OLD MYOCARDIAL INFARCTION PATIENTS UNDER ADEQUATE STATIN THERAPY

Kentaro Toyama, Osamu Sasaki, Toshihiko Nishioka and Hiroyuki Ito
Department of cardiology, Saitama Medical Center, Saitama Medical University, Kawagoe, Japan

J Am Coll Cardiol, 2012; 59:1773, doi:10.1016/S0735-1097(12)61774-4
© 2012 by the American College of Cardiology Foundation

Eicosapentaenoic acid (EPA) is reported to augment endothelial function and improve clinical outcomes in patients with coronary artery disease. However, it is unclear whether the effect of EPA is preserved even in patients under adequate statin therapy as secondary prevention. We hypothesized that EPA could improve endothelial function in old myocardial patients (OMI) with adequate lipid-lowering treatment using statin.
Fifty-five OMI patients under statin treatment with serum LDL cholesterol levels less than 100 mg/dl were randomly assigned to receive either 1800 mg of EPA daily with statin (EPA group, n=29) or statin alone (non-EPA group, n=26). Lipid profiles and flow-mediated dilation (FMD) were assessed just before and 6 months after the randomization in both groups.

EPA group presented significant increase in plasma concentrations of EPA (p<0.001). In EPA group, LDL-cholesterol and trygliceride levels significantly decreased (p<0.05), whereas no significant change was seen in non-EPA group. FMD, which is the primary end point of this study, showed significant improvement in EPA group (2.41±1.46% to 3.18±1.82%, p=0.001), while no significant change was seen in non-EPA group (2.51±1.48% to 2.25±1.42%, p=NS). Furthermore, FMD defined as post FMD - pre FMD significantly increased in EPA group (0.77±1.17 vs –0.25±1.59, p=0.009).

EPA further improved endothelial function in old myocardial infarction patients under adequate statin therapy.

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