Posts Tagged ‘highest concentration EPA’

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

Low levels of grey matter in brain linked to addiction

Thursday, December 1st, 2011

Gray matter in brains control center linked to ability to process reward
November 29th, 2011 in Neuroscience

In 2007 there was the first scientific evidence that clearly showed a direct co- relation between low omega 3 consumption and lower levels of grey matter in brain research showedthat raising omega-3 intake leads to structural brain changes.researchers reported that people who had lower blood levels of omega-3 fatty acids were more likely to have a negative outlook and be more impulsive.
Conversely, those with higher blood levels of omega-3s were found to be more agreeable and less likely to report mild or moderate symptoms of depression. The scientific researchers discovered that participants who had high levels of long-chain omega-3 fatty acid intake had higher volumes of grey matter in areas of the brain associated with emotional arousal and regulation — the bilateral anterior cingulate cortex, the right amygdala and the right hippocampus.This finding suggests that omega-3s may promote structural improvement in areas of the brain related to mood and emotion regulation — the same areas where grey matter is reduced in people who have mood disorders such as major depressive disorder .A study published last year found a direct correlation between the supplementation of omega 3 fatty acids and a decrease in anger and anxiety among substance abusers who had psychiatric problems.

Moving forward to 2012 we know through research that omega3 essential fatty acids pay a critical role in brain function and the following piece of research now links low grey matter with reduced levels of dopamine which has major implications with regards addiction therapy.Omega 3’s especially EPA and DHA are a major component of brain cells , they are also key to the proper function of the two brain chemical signalling systems dopamine and serotonin which have been implicated in mental health, addiction , behavioural conditions, Omega 3 fish oil also boosts levels of glutathione and anto oxidant that protects the brain against oxidadtive stress .

The more gray matter you have in the decision-making, thought-processing part of your brain, the better your ability to evaluate rewards and consequences. That may seem like an obvious conclusion, but a new study conducted at the U.S. Department of Energy’s Brookhaven National Laboratory is the first to show this link between structure and function in healthy people – and the impairment of both structure and function in people addicted to cocaine. The study appears in the Journal of Cognitive Neuroscience.

” This study documents for the first time the importance to reward processing of gray matter structural integrity in the parts of the brain’s prefrontal cortex that are involved in higher-order executive function, including self-control and decision-making,” said Muhammad Parvaz, a post-doctoral fellow at Brookhaven Lab and a co-lead author on the paper.

“Previous studies conducted at Brookhaven and elsewhere have explored the structural integrity of the prefrontal cortex in drug addiction and the functional components of reward processing, but these studies were conducted separately,” Parvaz said. “We wanted to know whether the specific function of reward processing could be ‘mapped’ onto the underlying brain structure – whether and how these two are related,” he added.

Differences in gray matter volume – the amount of brain matter made up of nerve cell bodies, as opposed to the “white matter” axons that form the connections between cells – have been observed in a range of neuropsychiatric diseases when compared with healthy states, explained Anna Konova, the other co-lead author on the paper. “We wanted to know more about what these differences mean functionally in healthy individuals and in drug-addicted individuals,” she said.

To explore this structure-function relationship, the scientists performed magnetic resonance imaging (MRI) brain scans to measure brain volume in 17 healthy people and 22 cocaine users. The scans collect structural measurements for the entire brain, and can be analyzed voxel-by-voxel – the equivalent of three-dimensional pixels – to get detailed measurements for individual brain regions.

Within a short period of the MRI scans, the scientists also used electrodes placed on the research subjects’ scalps to measure a particular electrical signal known as the P300 (an event-related potential derived from an ongoing electroencephalogram, or EEG, that is time-locked to a particular event). This specific measure can index brain activity related to reward processing. During these electrical recordings, the subjects performed a timed psychological task (pressing buttons according to a specific set of rules) with the prospect of earning varying levels of monetary reward, from no money up to 45 cents for each correct response with a total potential reward of $50.

Previous studies by the research team have shown that, in healthy subjects, the P300 signal increases in magnitude with the amount of monetary reward offered. Cocaine-addicted individuals, however, do not exhibit this differential response in the P300 measure of brain activity, even though they, like the healthy subjects, rate the task as more interesting and exciting when the potential reward is greater.

The current study extended these results by linking them for the first time with the structural measurements.

The scientists used statistical methods to look for correlations between the difference in brain activity observed in the high-reward and no-reward conditions – how much the brain’s P300 response changed with increasing reward – and the gray matter volume in various parts of the brain as measured voxel-by-voxel in the MRI scans.

In the healthy subjects, the magnitude of change in the P300 signal with increasing reward was most strongly correlated with the volume of gray matter in three regions of the prefrontal cortex.

“The higher the gray matter volume in those particular regions, the more brain activity increased for the highest monetary reward as compared to the non-reward condition,” Konova said.

The cocaine-addicted individuals had reduced gray matter volume in these regions compared with the healthy subjects, and no detectable differences between the reward conditions in the P300 measure of brain activity. There were also no significant correlations between the former and latter – structure and function measures – in the cocaine-addicted subjects.

” These findings suggest that impaired reward processing may be attributed to deficits in the structural integrity of the brain, particularly in prefrontal cortical regions implicated in higher order cognitive and emotional function,” Parvaz said. “This study therefore validates the use of the structural measures obtained by MRI as indicative of functional deficits.”

The implications are important for understanding the potential loss of control and disadvantageous decision-making that can occur in people suffering from drug addiction, Konova explained: “These structure-function deficits may translate into dysfunctional behaviors in the real world. Specifically, impaired ability to compare rewards, and reduced gray matter in the prefrontal cortex, may culminate in the compromised ability to experience pleasure and to control behavior, especially in high-risk situations – for example, when craving or under stress – leading individuals to use drugs despite catastrophic consequences.”

The authors acknowledge that there are still questions about whether these changes in brain structure and function are a cause or a consequence of addiction. But the use of multimodal imaging techniques, as illustrated by this study, may open new ways to address these and other questions relevant to understanding human motivation in both health and disease states, with particular relevance to treating dr

Omega 3 EPA the key omega3 to tackle obesity and type 2 diabetes

Saturday, October 8th, 2011

A major risk factor for cardiovascular disease, type 2 diabetes
and other pro inflammatory life-threatening conditions is the current obesity epidemic which is endemic in developed nations such as United States , United Kingdom , UAE where it’s fueled in large part by excessive consumption of a fat-rich “Western style diet.” The main issue is the increase consumption of saturated fats which are pro inflammatory ie animal fats , sunflower oil , corn oil etc Animal-derived saturated fats like lard and butter are strongly linked to adverse health effects, but unsaturated and polyunsaturated fats from plants and cold-water fish like salmon and mackerel are not. In fact, eating oily fish which is rich in omega3 especially EPA produces beneficial health effects and can reduce the risk of cardiovascular disease and diabetes
For biomedical investigators, the enduring question has been why saturated and unsaturated fatty acids produce such diametrically opposed health effects. Now, in a paper published in the Sept. 30 issue of the journal Cell, researchers at the University of California San Diego School of Medicine and colleagues offer an explanation, and a framework that could lead to dietary supplements designed to treat obesity at the molecular level.

“These findings not only explain the long-standing enigma regarding the differential health effects of saturated and unsaturated fatty acids,” said senior author Michael Karin, PhD, Distinguished Professor of Pharmacology in UC San Diego’s Laboratory of Gene Regulation and Signal Transduction, “they also provide improved tools and a mechanistic framework for the potential development of dietary supplements to treat obesity, estimated to be worth billions of dollars per year.”

Senior author Karin, first author Ryan G. Holzer, PhD, formerly a graduate student in Karin’s lab and now at the Mayo Clinic, and colleagues began with the observation that saturated fatty acids, such as palmitic acid, are potent activators of Jun kinases (JNK), key regulatory molecules implicated in the development of type 2 diabetes, insulin resistance, obesity and atherosclerosis. However, unsaturated fatty acids such as palmitoleic acid (POA) and eicosapentaenoic acid (EPA) not only do not activate JNK, but actually block JNK activation by palmitic acid.

Palmitic acid and POA differ in molecular structure by the presence of a single unsaturated bond (the absence of two hydrogen atoms) in POA. Cellular membrane fluidity is decreased upon incorporation of saturated fatty acids, which possess rigid hydrocarbon tails, but increased by the incorporation of unsaturated fatty acids with “bent” hydrocarbon tails.

Postulating that the membrane is the only cellular structure that can discriminate between all of these fatty acids, the scientists searched for membrane-associated protein kinases that could account for the differential effects on JNK activity. They ultimately identified c-Src, a membrane-associated tyrosine kinase, as the molecule responsible for activation of JNK by palmitic acid and other saturated fatty acids. They also discovered that saturated fatty acids “push” c-Src into membrane sub-domains of reduced fluidity and increased rigidity, where it accumulates in an activated form that eventually leads to JNK activation.

By contrast, POA and EPA prevent these changes in the membrane distribution of c-Src and — by blocking c-Src aggregation — they inhibit its activation by saturated fatty acids.

Most of the research was conducted using cultured cells (fibroblasts) treated with individual or combined fatty acids, but the scientists also fed mice a high-fat diet (in which 60 percent of the calories were fat-derived) and reported similar c-Src accumulation within membrane subdomains of increased rigidity and JNK activation.

Currently, polyunsaturated fatty acids, such as EPA and structurally-related omega-3 fatty acids are used in the treatment of hyperlipidemia (high blood cholesterol levels) and may be effective in the treatment or prevention of type 2 diabetes. Karin said understanding how EPA works could lead to the identification of even more potent EPA-like molecules.

Funding for this research came from the National Institutes of Health, the Superfund Basic Research Program and the American Diabetes Association.

Co-authors of the paper are Eek-Joong Park, Ning Li, Helen Tran, Monica Chen and Crystal Choi, Laboratory of Gene Regulation and Signal Transduction, Department of Pharmacology, UC San Diego; and Giovanni Solinas, Laboratory of Metabolic Stress Biology, Department of Medicine, Physiology, University of Fribourg, Switzerlan

Consumption Of Omega-3 essential Fatty acid fish oils Decrease Homocysteine Levels In Diabetic Patients

Friday, July 29th, 2011

Consumption Of Omega-3 FAs Decrease Homocysteine Levels In Diabetic Patients
Pooya S, Jalali MD, Jazayery AD, et al. The efficacy of omega-3 fatty acid supplementation on plasma homocysteine and malondialdehyde levels of type 2 diabetic patients. Nutr Metab Cardiovasc Dis. 2009;18.
BACKGROUND AND AIMS: Cardiovascular diseases are the major cause of mortality among diabetic patients. The concentration of malondialdehyde (MDA) and homocysteine is believed to play a role in cardiovascular diseases. Omega-3 fatty acid supplementation could be effective in some diabetes complications and in the control of the glycemic index. However, it may increase lipid peroxidation. The objective of this study was to determine the effect of omega-3 fatty acids on the concentration of homocysteine and MDA in diabetic patients.

METHODS AND RESULTS: A randomized double-blind, placebo-controlled clinical trial was conducted on 81 patients with type 2 diabetes. The patients were randomly assigned to either the treatment or control groups. Each subject received three capsules of omega-3 fatty acids or a placebo every day for a period of 2months. The two groups were similar in terms of body mass index and food intake. At the beginning of the study and after 2months of supplementation their levels of HbA(1)c, homocysteine, MDA, C-reactive protein (CRP), total cholesterol, LDL-cholesterol and fasting blood sugar (FBS) were determined. Due to omega-3 fatty acid supplementation, homocysteine was changed significantly in both treatment and control groups up to -3.10mumol/L and 0.10mumol/L respectively, and HbA(1)c decreased by 0.75% in the treatment group and increased by 0.26% in the control group. However, the changes in fasting blood sugar (FBS), malondialdehyde (MDA), C-reactive protein (CRP), total cholesterol and LDL-cholesterol levels were not significant.

CONCLUSION: The consumption of omega-3 fatty acid supplements (3g/day) for 2months decreases the levels of homocysteine in diabetic patients with no change in FBS, MDA and CRP levels.

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