Posts Tagged ‘pharmaceutical grade omega3 fish oil’

Omega-3s intake Linked to Lower Amyloid Levels and reduced risk of Alzheimers

Monday, May 7th, 2012

A study of diet and plasma beta-amyloid in cognitively normal individuals over 65 found that increased consumption of omega-3 fatty acids was significantly associated with lower plasma levels of beta-amyloid protein 42.
Note that none of the other nutrients were found to have a significant association with plasma beta-amyloid.

People who had a lot of omega-3 fatty acids in their diets tended to have lower plasma levels of beta-amyloid proteins, possibly reducing their risk of Alzheimer’s disease, researchers said.

In a cross-sectional study of more than 1,200 cognitively normal individuals older than 65, omega-3 fatty acid intake was significantly predictive of plasma levels of the 40- and 42-residue forms of beta-amyloid protein (AB40 and AB42, respectively), according to Nikolaos Scarmeas, MD, of Columbia University in New York City, and colleagues.

Adjusting for age, education level, and other factors pushed the relationship between AB40 and omega-3 intake into a strong but nonsignificant trend (beta statistic -10.13, P=0.13). But the association with AB42 remained significant, Scarmeas and colleagues reported online in Neurology (beta statistic -7.70, P=0.02).

The same group had previously published results indicating that a Mediterranean-type diet was associated with lower risk of cognitive impairment and Alzheimer’s disease.

Because one of the hallmarks of Alzheimer’s disease is beta-amyloid plaque deposits in the brain, Scarmeas and colleagues sought to determine if dietary factors were related to blood levels of AB40 and AB42.

Their study population was drawn from participants in the Washington Heights/Hamilton Heights Columbia Aging Project in New York City, first recruited in 1992 with a second group enrolled in 1999.

As part of this study, participants completed a detailed diet questionnaire and also provided blood samples. The latter were drawn a mean of 1.2 years after collection of dietary information.

The researchers excluded participants already showing dementia when the dietary questionnaire was administered, since their mental status could affect their self-reporting on diet.

A total of 1,219 participants out of the original 2,778 were included in the current analysis. In addition to 345 with prevalent dementia, another 1,025 could not be included because beta-amyloid levels in plasma weren’t measured.

In addition to omega-3 intake, Scarmeas and colleagues also estimated intake of nine other nutrients: folate, beta-carotene, monounsaturated fats, saturated fats, omega-6 fatty acids, and vitamins C, D, E, and B12.

Only omega-3 intake was significantly associated with plasma AB40 or AB42 levels in any analysis.

The raw data suggested a powerful link:

AB40: beta -24.74, P<0.001

AB42: beta -12.31, P<0.001

But analysis of participant characteristics revealed a number of covariates. Adjusting for age, race-ethnicity, education level, APOE genotype, total caloric intake, and recruitment wave attenuated the relationships noticeably. The beta value for AB40 shrank to -11.96 and the P value increased to 0.06.

The beta value for AB42 also declined, to -7.31, but it remained significant at P=0.02.

Adding adjustments for alcohol drinking and use of certain drugs and nutritional supplements changed the strength of the associations only slightly.

The researchers' conclusion: "The potential beneficial effects of omega-3 [fatty acid] intake on Alzheimer's disease and cognitive function in the literature might be at least partly explained by an AB-related mechanism," they wrote.

Scarmeas and colleagues noted several limitations to the study, including its cross-sectional design and its reliance on a single measurement of plasma AB40 and AB42 levels, which they characterized as "a moving target" during development of cognitive decline.

Also, the researchers relied on participants' self-reports on diet and examined only 10 of many nutrients contained in food.

Finally, Scarmeas and colleagues acknowledged that plasma beta-amyloid proteins do not necessarily reflect amyloid protein levels in the brain.

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

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.

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.

OBJECTIVE:
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).

METHODS:
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.

RESULTS:
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.
CONCLUSION:
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.

What is pharmaceutical grade omega 3 fish oil

Sunday, January 22nd, 2012

Omega3
What is Pharmaceutical Grade Omega3 Fish Oil and why is Takeomega3 different from other brands ?
Pharmaceutical Grade Fish Oil
The true definition is an oil of concentration 80% -90% omega 3 such as TakeOmega3. There are a lot of omega3 products that claim to be pharmaceutical grade when they are not . Looking on the rear label makes everything clear
The majority of omega3 products on shelf are what we define as 18/12 this means 18% EPA and 12%DHA making a total of 30% omega 3. The remaining 70% is made up of monounsaturated,polyunsaturated and saturated fats. Your body has no need for these.
18/12 products are usually advertised as “1000mg Omega3” and they will have only 30% omega3 – giving a total of 300mg omega3 split 180mg EPA and 120 DHA.
Compare that to TakeOmega3 with 750mg EPA and 50mg DHA an 85% concentrate .

Benefits of Pharmaceutical Grade Fish oil such as TakeOmega3 85% Omega3
• 80% and above Omega3
• Virtually no environmental toxins the repeated molecular distillation necessary to achieve high concentrations removes virtually all toxins and heavy metals ie mercury
• Ultra purity reduces fish odour often associated with low concentration formulations
• An easy way to get high doses of omega3 with just one or two capsules as opposed to 10 capsules of low concentration brands.
• Research has shown low concentration capsules are not as effective as single dose pharmaceutical omega3 even when taking multiple capsules.
• The Omega3 fish oils used in Clinical trials / research the majority of the time pharmaceutical grade therefore why would you choose to take a low concentration oil
• You actually feel a difference .

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