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Omega3 with levels 80% + active ingredients EPA/DHA show that healthy young adults can improve their working memory by omega3 supplementation

Wednesday, October 31st, 2012

In the first study of its kind, researchers at the University of Pittsburgh have determined that healthy young adults ages 18-25 can improve their working memory even further by increasing their Omega-3 fatty acid intake. Their findings have been published online in PLOS One.

“Before seeing this data, I would have said it was impossible to move young healthy individuals above their cognitive best,” said Bita Moghaddam, project investigator and professor of neuroscience. “We found that members of this population can enhance their working memory performance even further, despite their already being at the top of their cognitive game.”

Led by Rajesh Narendarn, project principal investigator and associate professor of radiology, the Pitt research team sought healthy young men and women from all ethnicities to boost their Omega-3 intake with supplements for six months. They were monitored monthly through phone calls and outpatient procedures.

Before they began taking the supplements, all participants underwent positron emission tomography (PET) imaging, and their blood samples were analyzed. They were then asked to perform a working memory test in which they were shown a series of letters and numbers. The young adults had to keep track of what appeared one, two, and three times prior, known as a simple “n-back test.”

“What was particularly interesting about the presupplementation n-back test was that it correlated positively with plasma Omega-3,” said Moghaddam. “This means that the Omega-3s they were getting from their diet already positively correlated with their working memory.”

After six months of taking a clinical grade Omega-3 supplement > 80% in active ingredients approved by the Food and Drug Administration—the participants were asked to complete this series of outpatient procedures again. It was during this last stage, during the working memory test and blood sampling, that the improved working memory of this population was revealed.

“So many of the previous studies have been done with the elderly or people with medical conditions, leaving this unique population of young adults unaddressed,” said Matthew Muldoon, project coinvestigator and associate professor of medicine at Pitt. “But what about our highest-functioning periods? Can we help the brain achieve its full potential by adapting our healthy behaviors in our young adult life? We found that we absolutely can.”

Although the effects of Omega-3s on young people were a focus, the Pitt team was also hoping to determine the brain mechanism associated with Omega-3 regulation. Previous rodent studies suggested that removing Omega-3 from the diet might reduce dopamine storage (the neurotransmitter associated with mood as well as working memory) and decrease density in the striatal vesicular monoamine transporter type 2 (commonly referred to as VMAT2, a protein associated with decision making). Therefore, the Pitt researchers posited that increasing VMAT2 protein was the mechanism of action that boosted cognitive performance. Unfortunately, PET imaging revealed this was not the case.

“It is really interesting that diets enriched with Omega-3 fatty acid can enhance cognition in highly functional young individuals,” said Narendarn. “Nevertheless, it was a bit disappointing that our imaging studies were unable to clarify the mechanisms by which it enhances working memory.”

Ongoing animal modeling studies in the Moghaddam lab indicate that brain mechanisms that are affected by Omega-3s may be differently influenced in adolescents and young adults than they are in older adults. With this in mind, the Pitt team will continue to evaluate the effect of Omega-3 fatty acids in this younger population to find the mechanism that improves cognition.

Other Pitt researchers involved in the project include William G. Frankle, professor of psychiatry, and Neal S. Mason, research assistant professor of radiology.

The paper, “Improved Working Memory but No Effect on Striatal Vesicular Monoamine Transporter Type 2 after Omega-3 Polyunsaturated Fatty Acid Supplementation” was published online Oct. 3 by PLOS One and supported by grants from the National Institute on Drug Abuse and the American Reinvestment and Recovery Act of 2009.

Poor diet during pregnancy increases offspring’s vulnerability to the effects of aging, new research has shown for the first time-Omega 3 are essential for healthy development

Saturday, July 16th, 2011

h, by scientists from the University of Cambridge, provides important insight into why children born to mothers who consumed an unhealthy diet during pregnancy have an increased risk of type 2 diabetes (a significant contributing factor to heart disease and cancer) later in life. Low levels of essential fatty acids can have a major impact , the key omega 3 ’s EPA and DHA are essential as the body needs to take these from diet . Fears of heavy metal contamination are often linked to mothers not wishin to consume adequate levels of fish during pregnancy , the alternative is to take a daily high quality omega3 supplement that provides concentrated levels of EPA and DHA. TakeOmega3 is a true one per day capsule and gives a minimum of 750mg EPA and 50 mg DHA per capsule .Omega 3 fatty acids EPA and DHA are linked to lower incidence of heart disease , protection against risk of Cancer , lower incidence and preventio of type 2 diabetes
“What is most exciting about these findings is that we are now starting to really understand how nutrition during the first nine months of life spent in the womb shape our long term health by influencing how the cells in our body age,” said Dr Susan Ozanne, the senior author on the paper and British Heart Foundation Senior Fellow from the Institute of Metabolic Science at the University of Cambridge.
It is well established that environmental factors interact with genes throughout life, affecting the expression of those genes and, consequently, tissue function and disease risk. Diet during critical periods of development, such as during the nine months in the womb, has been cited as one such environmental factor. Epigenetics, which refers to modifications to the DNA that regulate how much of a gene is produced, has been suggested to underlie these effects.
However, until now, very little was understood about the underlying mechanisms that control the interaction between diet during gestation and gene expression in offspring throughout their adult life. Research, funded by the BBSRC and the British Heart Foundation, has now shown that the gene Hnf4a, which has been linked to type 2 diabetes, is regulated by maternal diet through epigenetic modifications to our DNA. Additionally, they found that poor diet exacerbates the rate at which these key epigenetic modifications accumulate during the aging process.
Previous research has shown that the gene Hnf4a plays an important role both during development of the pancreas and later in the production of insulin. The researchers hypothesised that diet during pregnancy influences the expression of this gene later in life, thereby influencing the risk of diabetes.
To test their theory, the researchers used a well-established rat model where, by altering the protein content of the mother’s diet during pregnancy, the offspring develop type 2 diabetes in old age.
First, they studied the RNA from insulin secreting cells in the pancreas from offspring of normally fed as well as malnourished mothers in young adult life and in old age. When they compared the two, they found that there was a significant decrease in the expression of the Hnf4a gene in the offspring prone to type 2 diabetes. The expression of Hnf4a also decreased with age in both groups.
Second, they studied the DNA and found that the decrease of Hnf4a was caused by epigenetic changes. The age associated epigenetic silencing was more pronounced in rats exposed to poor maternal diet. They concluded that the epigenetic changes resulting from maternal diet and aging lead to the reduced expression of the Hnf4a gene, decreasing the function of the pancreas and therefore its ability to make insulin (and thereby increasing the risk of diabetes).
The scientists then studied the DNA from insulin secreting cells from human pancreases to show that expression of this important gene was controlled in the same way in humans.
“It is remarkable that maternal diet can mark our genes so they remember events in very early life,” said Dr Miguel Constancia, the senior co-author on the paper from the Department of Obstetrics and Gynaecology and Metabolic Research Laboratories at the University of Cambridge. “Our findings reveal a novel mechanism by which maternal diet and aging interact through epigenetic processes to determine our risk of age-associated diseases.”
Professor Jeremy Pearson, Associate Medical Director at the British Heart Foundation, said: “We already know that a healthy pregnancy is important in shaping a child’s health, and their risk of heart disease as they grow up. The reasons why are not well understood, but this study in rats adds to the evidence that a mother’s diet may sometimes alter the control of certain genes in her unborn child. It’s no reason for expectant mothers to be unduly worried. This research doesn’t change our advice that pregnant women should try to eat a healthy, balanced diet.”
Professor Douglas Kell, Chief Executive, BBSRC said: “Epigenetics is a relatively young field of research with tremendous potential to underpin our understanding of many biological processes in all organisms. The fact that there is a relationship between the biology of a pregnant mother and the long term health of her child has been known for some time but our understanding of the biological processes behind some of the more subtle effects is still at a nascent stage. This study uncovers — through epigenetics and molecular biology research — an important piece of this puzzle and shows us how apparently minor changes within cells at the very earliest stages of development can have a major influence on our health into

Deficiency of Omega 3 fish oil in the diet may explain high rates of depression

Friday, July 15th, 2011

Deficiency of Dietary Omega-3 May Explain Depressive Behaviors
— How maternal essential fatty acid deficiency impact on its progeny is poorly understood. Dietary insufficiency in omega-3 fatty acid has been implicated in many disorders. Researchers from Inserm and INRA and their collaborators in Spain collaboration, have studied mice fed on a diet low in omega-3 fatty acid. They discovered that reduced levels of omega-3 had deleterious consequences on synaptic functions and emotional behaviours.

TakeOmega has the highest levels of EPA per capsule available globally , EPA has been found to be as effective as Prozac in the treatment of medium to severe depression . It is manufactured entirely in the UK and each capsules has over 950mg Omega 3 , other brands are as low as 15% in active ingredients.
Details of this work are available in the online version of the journal Nature Neuroscience.
In industrialized nations, diets have been impoverished in essential fatty acids since the beginning of the 20th century. The dietary ratio between omega-6 polyunsaturated fatty acid and omega-3 polyunsaturated fatty acid omega-3 increased continuously over the course of the 20th century. These fatty acids are “essential” lipids because the body cannot synthesize them from new. They must therefore be provided through food and their dietary balance is essential to maintain optimal brain functions.
Olivier Manzoni (Head of Research Inserm Unit 862, “Neurocentre Magendie,” in Bordeaux and Unit 901 “Institut de Neurobiologie de la Méditerranée” in Marseille), and Sophie Layé (Head of Research at INRA Unit 1286, “Nutrition et Neurobiologie Intégrative” in Bordeaux) and their co-workers hypothesized that chronic malnutrition during intra-uterine development, may later influence synaptic activity involved in emotional behaviour (e.g. depression, anxiety) in adulthood.
To verify their hypotheses, the researchers studied mice fed a life-long diet imbalanced in omega-3 and omega-6 fatty acids. They found that omega-3 deficiency disturbed neuronal communication specifically. The researchers observed that only the cannabinoid receptors, which play a strategic role in neurotransmission, suffer a complete loss of function. This neuronal dysfunction was accompanied by depressive behaviours among the malnourished mice.
Among omega-3 deficient mice, the usual effects produced by cannabinoid receptor activation, on both the synaptic and behavioural levels, no longer appear. Thus, the CB1R receptors lose their synaptic activity and the antioxidant effect of the cannabinoids disappears.
Consequently, the researchers discovered that among mice subjected to an omega-3 deficient dietary regime, synaptic plasticity, which is dependent on the CB1R cannabinoid receptors, is disturbed in at least two structures involved with reward, motivation and emotional regulation: the prefrontal cortex and the nucleus accumbens. These parts of the brain contain a large number of CB1R cannabinoid receptors and have important functional connections with each other.
“Our results can now corroborate clinical and epidemiological studies which have revealed associations between an omega-3/omega-6 imbalance and mood disorders,” explain Olivier Manzoni and Sophie Layé

Omega 3 fish oil may help activate anti-diabetic genes

Tuesday, March 8th, 2011

Fish oils may help to activate anti-diabetic genes

Polyunsaturated fatty acid fish oils may activate genes that regulate fat cell differentiation and glucose homeostasis, according to new research on mice.

The new study published in Journal of Nutritional Biochemistry suggests supplementation with omega3 fish oil activates the transcription factor PPARγ, increasing regulation of adipocytes and helps to maintain glucose homeostasis.

“We demonstrated that adipogenic genes and glucose metabolism genes were elevated in PPARγ transgenic mice when fed fish oil. This transgenic mouse model provided direct evidence to demonstrate omega 3 , especially EPA  regulate glucose homeostasis through interaction with PPARγ,” wrote the researchers, led by Dr Yu-Hsiang Yu from the National Taiwan University

Vital roles

Peroxisome-proliferator-activated receptor γ (PPARγ) is considered an important transcription factor in regulating fat cell (adipocyte) differentiation, and is also known to play a vital role in maintaining glucose homeostasis. The transcription factor is a target for many anti-diabetic drugs as activation promotes glucose dispersal.

Activation of PPARγ occurs through the binding of specific ligand molecules; however, polyunsaturated fatty acids such as arachidonic acid, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are also known to have a high binding affinity for PPARγ.

Previous studies suggest that polyunsaturated fatty acids (PUFA) and their metabolites are able to regulate PPARγ activity, demonstrating that DHA treatment increases PPARγ-responsive gene expression in a cell model.

However, most research demonstrating PPARγ activity uses in vitro cell models and there is currently no direct evidence available to demonstrate that polyunsaturated fatty acids are able to activate PPARγ in vivo.

The authors said the current experiment was designed to determine the potential for PUFA, particularly EPA and DHA, to activate the function of PPARγ in vivo.

Wild-type and transgenic mice – with over expressed PPARγ –were supplemented with either fish oil or PPARγ ligands (rosiglitazone) for four months to investigate whether fish oils have similar effects to true PPARγ ligands in vivo.

Results

Dietary rosiglitazone fed mice had a significantly lower feed intake, but had no significant effect on body weight or fat pad weigh, whereas fish oil supplementation did not significantly decrease feed intake, but significantly decreased body and fat pad weight, found the researchers.

Dr. Yu and colleagues reported that adipogenic genes (LPL, FAT, SREBP-1c and FAS) were markedly up-regulated by rosiglitazone supplementation. Fish oil supplementation increased LPL and FAT, but not SREBP-1c or FAS; however, stained muscle sections indicated no lipid accumulation in skeletal muscle.

Researchers noted that transgenic mice fed a fish oil supplementation had increased expression of adipogenic and glucose uptake genes, leading to reduced plasma glucose concentration.

Natural regulator

The authors suggested that polyunsaturated fatty acids, particularly EPA and DHA, may serve as a natural regulator of glucose uptake in vivo, stating that such effects are mainly mediated through PPARγ activation.

“Our data demonstrated that the PPARγ-regulated glucose metabolism genes, GLUT-4 and ADN were dramatically increased in skeletal muscle of PPARγ transgenic mice when fed rosiglitazone or fish oil, suggesting activation … by either ligand,” concluded the authors.

Source: Journal of Nutritional Biochemistry

“The function of porcine PPARγ and dietary fish oil effect on the expression of lipid and glucose metabolism related genes”

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