Archive for October, 2011

Risk of SSRI / Anti Depressants during pregnancy is there a link to Autism ? Are there alternatives ?

Tuesday, October 25th, 2011

A new study has suggested that women who take SSRI’s during pregnancy may be putting their unborn child at risk of developmental problems . This latest research has raised questions about the impact of SSRI’s during pregnancy . As you will see from other research omega 3 EPA has been found to be as effective as  SSRI’S  ie Prozac  in the treatment of  medium to severe depression – DHA in similar studies has not been effective .TakeOmega3 offers the highest concentration of EPA  available and at 85% concentrate it means highest purity with 750mg EPA per capsule – no other product offers the purity of TakeOmega3 . As well as that it is the only brand used by  certain NHS Psychotherapy services , obviously under no circumstances should anyone currently on SSRI’s stop taking them however if you are concerned you should consult your GP to discuss any concerns you may have .

So what is an SSRI
SSRI’s is the shortened form of Selective serotonin reuptake inhibitors Many of the SSRIs have become common household names, such as Prozac (fluoxetine), Paxil (paroxetine) and Zoloft (sertraline).
In the study scientists treated more than 200 rats with the selective serotonin reuptake inhibitor citalopram during key stages of brain development.
A study by researchers at the University of Mississippi Medical Center and the University of California, San Francisco shows that rats given a popularly prescribed antidepressant during development exhibit brain abnormalities and behaviors characteristic of autism spectrum disorders.

The findings suggest that taking a certain class of antidepressants known as selective serotonin reuptake inhibitors – SSRIs – during pregnancy might be one factor contributing to a dramatic rise in these developmental disorders in children.

“We saw behaviors in the treated rats and neurological problems that indicate their brains are not properly conducting and processing information,” said Dr. Rick C.S. Lin, professor of neurobiology and anatomical sciences at UMMC and principal investigator on the study.

“However, based on this study alone it would be premature to conclude that a pregnant mother should stop taking SSRIs. A pregnant mother may do more harm to her baby through untreated depression than by taking prescribed SSRIs. This study is a starting point and a lot more research needs to be done.”

The study appears online Oct. 24, 2011 in the journal Proceedings of the National Academy of Sciences at www.pnas.org.

The researchers treated more than 200 rats with the SSRI citalopram during key stages of brain development. Rats are born at an earlier developmental stage than humans, equivalent to the end of the sixth month of fetal development in humans.

Most rats received treatment for two weeks, beginning eight days post birth, a neurodevelopment period equivalent to the third trimester and early infancy in humans.

In contrast with control-group rats, the investigators found the treated populations were uninterested in play when young and displayed poor social behaviors as adults. The treated rats also showed abnormal responses to changes in their environment. For example, they froze at the sound of a novel tone and showed little interest in exploring new toys.

“These results demonstrate that rat pups, when exposed perinatally to SSRIs, exhibit behavioral traits often seen in ASD,” said Dr. Kimberly Simpson, the paper’s first author and UMMC associate professor of neurobiology and anatomical sciences.

Those behaviors occurred more often – and sometimes exclusively – in the treated male rats than in treated females. Similarly, autism spectrum disorder, or ASD, is diagnosed more often in males.

Of numerous SSRIs available, the researchers chose citalopram because it is one of the most specific in targeting the serotonin system with little overlap on other neurotransmitters.

Michael Merzenich, UCSF professor of otolaryngology and physiology, analyzed the rats’ primary auditory cortices using electrophysiologic techniques. In the treated, month-old rats Merzenich found functional abnormalities consistent with ASD.

“What we see in this experiment is a strong impact on the auditory cortex. These animals are not maturing in the normal, progressive way, and those differences are substantial,” said Merzenich, a senior author on the paper. “The cortex is sluggish and represents sounds with low accuracy. The listening cortex is delayed in development and is impaired into adulthood.”

Delayed development of the representation of aural speech is a hallmark of ASD in children, Merzenich said. It contributes to these children’s struggles with language and reading.

Another brain abnormality common in ASD is a thinner corpus callosum, particularly in the forward third of the structure. Like a massive nerve-fiber bridge, the corpus callosum connects the brain’s two halves and transmits electrical signals between them. It also plays a key part in higher intellectual function, said Dr. Ian Paul, UMMC professor of psychiatry and human behavior.

“This nerve fiber tract was disrupted in the same way in these rats’ brains,” he said.

Many callosal axons in the treated rats had abnormal or missing myelin sheathing, a coating necessary for proper neuroconductivity. Omega3 especially EPA is believed to be critical with regards the myelin sheaths ,Myelin is an insulating layer that forms around nerves, including those in the brain and spinal cord. It is made up of protein and fatty substances.
The purpose of the myelin sheath is to allow impulses to transmit quickly and efficiently along the nerve cells. If myelin is damaged, the impulses slow down.It is believed the omega3 active ingredients ie EPA not only acts as an anti inflammatory but also helps repair damage to the brain by promoting neuronal growth.

“Without that myelin wrapping the signal slows or doesn’t get through at all. The abnormalities in these rats would suggest the left and right sides of their brains are not communicating properly,” said Paul, a senior co-author on the paper.

Lin said the researchers analyzed multiple aspects – behavior, pathology, brain morphology, neurochemistry and neurophysiology – to conduct a broad survey and get a sense of structural and functional abnormalities.

A $1.3 million grant to Lin from the National Institute of Mental Health funded the study.

The study in rats follows an epidemiologic study in humans, published in July in the Archives of General Psychiatry. That investigation found that children of mothers who took SSRIs during the year prior to giving birth ran twice the normal risk of developing autism.

“While one must always be cautious extrapolating from medication effects in rats to medication effects in people, these new results suggest an opportunity to study the mechanisms by which antidepressants influence brain and behavioral development,” said Dr. Thomas R. Insel, director of the NIMH. “These studies will help to balance the mental health needs of pregnant mothers with possible increased risk to their offspring.”

The incidence of pregnant women taking SSRIs has grown from about .5 percent in 1985 when the first one came on the market to nearly 10 percent today, Paul said.

Autism was initially described in 1943 and through the next decades the parameters expanded. In 1996, the rate of incidence was less than 1 in 1,000 births and by 2007 it reached about 1 in 200. The rates of incidence of ASD have roughly doubled every three-to-five years to 1 in 91 currently, he said.

“The diagnosis has widened with the awareness that it’s a spectrum disorder that encompasses a whole range of communication problems, but that doesn’t account for all the increase by any means,” Paul said.

Merzenich said a genetic component for autism risk is found in certain families, more strongly expressed in some members than in others.

“Genetic weakness can put a child at risk for autism origin,” he said. The neurological distortions attributable to SSRIs plausibly add to the child’s neurological burdens. We think that SSRIs may thereby increase the risks of ASD. In any event, further study in child populations should determine if this is or is not the case.”

Lin cautioned that pregnant women shouldn’t quit taking prescribed antidepressants based solely on the study’s results.

“In this study we eliminated as many external factors as possible. But real-life situations are much more complex,” he said.

Stress hormones – which affect the same neurological systems as SSRIs – can also be detrimental to a developing baby, Simpson said, indicating another significant difference between the laboratory study and real-life situations.

“We intentionally looked for treatment effects in groups of rats that were considered normal at the beginning of the study and were birthed from normal mothers. The effects of SSRIs on babies carried by depressed mothers are not known,” she said.

Lin also emphasized the findings call for more study of SSRIs, particularly in humans.

“We need to know which one causes minimal damage but also at what dose, for how long and at what points in pregnancy. So basically, we still have a lot to learn,” he said.
He credited a multidisciplinary team of investigators for the work.
“This kind of work could never have been done in one lab,” Lin said. “It’s absolutely the result of a team approach that took people in pediatrics, pharmacology, neurobiology and anatomical sciences, psychiatry, physiology and otolaryngology.”

Omega-3 fatty acids for major depressive disorder associated with the menopausal transition: a preliminary open trial.

Sunday, October 23rd, 2011

Menopause – Omega-3 FA for Depression in Menopausal Transition
Freeman MP, Hibbeln JR, Silver M, et al. Omega-3 fatty acids for major depressive disorder associated with the menopausal transition: a preliminary open trial. Menopause.

OBJECTIVES: We sought to obtain preliminary data regarding the efficacy of omega-3 fatty acids for major depressive disorder associated with the menopausal transition. Secondary outcomes were assessed for vasomotor symptoms (or hot flashes).

METHODS: After a single-blind placebo lead-in, participants received 8 weeks of treatment with open-label omega-3 fatty acid capsules (eicosapentaenoic acid and docosahexaenoic acid, 2 g/d). The Montgomery-Asberg Depression Rating Scale (MADRS) was the primary outcome measure. Hot flashes were monitored prospectively using daily diaries and the Hot Flash Related Daily Interference Scale. Blood samples for plasma pretreatment and posttreatment essential fatty acid assays were obtained. Because of the small sample size, data were analyzed using nonparametric techniques.

RESULTS: Of 20 participants treated with omega-3 fatty acids, 19 (95%) completed the study. None discontinued because of adverse effects. The pretreatment and final mean MADRS scores were 24.2 and 10.7, respectively, reflecting a significant decrease in MADRS scores (P < 0.0001). The response rate was 70% (MADRS score decrease of ≥50%), and the remission rate was 45% (final MADRS score of ≤7). Responders had significantly lower pretreatment docosahexaenoic acid levels than nonresponders did (P = 0.03). Hot flashes were present in 15 (75%) participants. Among those with hot flashes at baseline, the number of hot flashes per day improved significantly from baseline (P = 0.02) and Hot Flash Related Daily Interference Scale scores decreased significantly (P = 0.006).

CONCLUSIONS: These data support further study of omega-3 fatty acids for major depressive disorder and hot flashes in women during the menopausal transition.

A study of the safety and harms of antidepressant drugs for older people: a cohort study using a large primary care database

Thursday, October 20th, 2011

he aim of this study was to establish the relative safety and balance of risks for antidepressant treatment in older people.

The cohort study included 60,746 patients aged 65 years and over diagnosed with depression. The study was based in 570 general practices in the UK supplying data to the QResearch database.

The study objectives were to:

* determine relative and absolute risks of predefined adverse events in older people with depression, comparing classes of antidepressant drugs:
o tricyclic and related antidepressants (TCAs)
o selective serotonin reuptake inhibitors (SSRIs)
o monoamine oxidase inhibitors (MAOIs)
o other antidepressants
o commonly prescribed individual drugs with non-use of antidepressant drugs
* directly compare the risk of adverse events for SSRIs with TCAs;
* determine associations with dose and duration of antidepressant medication;
* describe patterns of antidepressant use in older people with depression; and
* estimate costs of antidepressant medication and primary care visits.

There were 13 predefined outcome measures:

* all-cause mortality
* sudden cardiac death
* suicide
* attempted suicide/self-harm
* myocardial infarction
* stroke/transient ischaemic attack (TIA)
* falls
* fractures
* upper gastrointestinal bleeding
* epilepsy/seizures
* road traffic accidents
* adverse drug reactions
* hyponatraemia

Here’s what the study found:

* The associations with the adverse outcomes were significantly different between the classes of antidepressant drugs for seven outcomes
* SSRIs were associated with the highest adjusted hazard ratios (HRs) for falls [1.66, 95% confidence interval (CI) 1.58 to 1.73] and hyponatraemia (1.52, 95% CI 1.33 to 1.75)
* The group of other antidepressants was associated with the highest HRs for all-cause mortality (1.66, 95% CI 1.56 to 1.77), attempted suicide/self-harm (5.16, 95% CI 3.90 to 6.83), stroke/TIA (1.37, 95% CI 1.22 to 1.55), fracture (1.63, 95% CI 1.45 to 1.83) and epilepsy/seizures (2.24, 95% CI 1.60 to 3.15) compared with when antidepressants were not being used
* TCAs did not have the highest HR for any of the outcomes
* There were also significantly different associations between the individual drugs for seven outcomes, with trazodone, mirtazapine and venlafaxine associated with the highest rates for several of these outcomes
* The mean incremental cost (for all antidepressant prescriptions) ranged between £51.58 (amitriptyline) and £641.18 (venlafaxine) over the 5-year post-diagnosis period.

The authors concluded:

This study found associations between use of antidepressant drugs and a number of adverse events in older people.

There was no evidence that SSRIs or drugs in the group of other antidepressants were associated with a reduced risk of any of the adverse outcomes compared with TCAs; however, they may be associated with an increased risk for certain outcomes. Among individual drugs trazodone, mirtazapine and venlafaxine were associated with the highest rates for some outcomes. Indication bias and residual confounding may explain some of the study findings.

The risks of prescribing antidepressants need to be weighed against the potential benefits of these drugs.

CAC Coupland, P Dhiman, G Barton, R Morriss, A Arthur, T Sach and J Hippisley-Cox. A study of the safety and harms of antidepressant drugs for older people: a cohort study using a large primary care database (PDF). Health Technology Assessment 2011; Vol. 15: No. 28.

Women with low levels omega3 and high levels omega6 associated with a high risk of pre-eclampsia

Thursday, October 20th, 2011

One of the most common causes of premature birth in the UK, pre-eclampsia affects 70,000 British women every year.

There were 42 per cent more cases  of pre eclampsia in women who had conceived using IVF, the American Society for Reproductive Medicine’s annual conference  heard Women who undergo IVF are often older and as a result may have an increased risk of other health problems . The general population in UK has a diet high in the pro inflammatory omega6 ie sunflower oil and low in omega3 ie oily fish . In order to address this it maybe beneficial to eat more oily fish at least 2-3 times a week ie salmon , mackerel , sardines or take high concentrate omega3 supplement which is high in active ingredients EPA and DHA such as TakeOmega3 which offers the highest concentration globally

Preeclampsia is a systemic disease characterized by diffuse endothelial dysfunction, increased peripheral vascular resistance, coagulation abnormalities, antioxidant deficiency, persistent elevations of maternal leukocyte-derived cytokines, and hyperlipidemia. Fish oil, rich in omega-3 polyunsaturated fatty acids, is known to reduce fasting and postprandial triglycerides and to decrease platelet and leukocyte reactivity; it may also decrease blood pressure. Additionally, omega-3 fatty acids may beneficially influence vessel wall characteristics and blood rheology. In light of the potential beneficial effects of dietary omega-3 fatty acids, we conducted a cross-sectional case-control study to examine the hypothesized exposure-effect relation between maternal dietary intake of marine omega-3 fatty acids and risk of preeclampsia. We measured polyunsaturated fatty acids in erythrocytes obtained from 22 preeclamptic women and 40 normotensive women; we measured polyunsaturated fatty acids as the percentage of total fatty acids from gas chromatography. We employed logistic regression procedures to estimate odds ratios (ORs) and 95% confidence intervals (CIs). After adjusting for confounders, women with the lowest levels of omega-3 fatty acids were 7.6 times more likely to have had their pregnancies complicated by preeclampsia as compared with those women with the highest levels of omega-3 fatty acids (95% CI = 1.4-40.6). A 15% increase in the ratio of omega-3 to omega-6 fatty acids was associated with a 46% reduction in risk of preeclampsia (OR = 0.54; 95% CI = 0.41-0.72). Low erythrocyte levels of omega-3 fatty acids and high levels of some omega-6 fatty acids, particularly arachidonic acid, appear to be associated with an increased risk of preeclampsia.Women

Omega-3 fatty acids in maternal erythrocytes and risk of preeclampsia.
Williams MA, Zingheim RW, King IB, Zebelman AM.
Source
Center for Perinatal Studies, Swedish Medical Center/Seattle, WA 98114-0999, USA.

University of Bristol Research has shown that omega3 fatty acids substantially reduce the signs and symptoms of bone density loss

Wednesday, October 19th, 2011

New research has shown for the first time that omega-3 in fish oil could “substantially and significantly” reduce the signs and symptoms of osteoarthritis.

According to the University of Bristol study, funded by Arthritis Research UK and published in the journal Osteoarthritis and Cartilage, omega-3-rich diets fed to guinea pigs, which naturally develop osteoarthritis, reduced disease by 50 per cent compared to a standard diet.

The research is a major step forward in showing that omega-3 fatty acids, either sourced from fish oil or flax oil, may help to slow down the progression of osteoarthritis, or even prevent it occurring, confirming anecdotal reports and “old wives’ tales” about the benefits of fish oil for joint health.

Lead researcher Dr John Tarlton, from the Matrix Biology Research group at the University of Bristol’s School of Veterinary Sciences, said classic early signs of the condition, such as the degradation of collagen in cartilage and the loss of molecules that give it shock-absorbing properties, were both reduced with omega-3.

“Furthermore, there was strong evidence that omega-3 influences the biochemistry of the disease, and therefore not only helps prevent disease, but also slows its progression, potentially controlling established osteoarthritis,” he said.

Dr Tarlton added: “The only way of being certain that the effects of omega-3 are as applicable to humans as demonstrated in guinea pigs is to apply omega-3 to humans. However, osteoarthritis in guinea pigs is perhaps the most appropriate model for spontaneous, naturally occurring osteoarthritis, and all of the evidence supports the use of omega-3 in human disease.”

Medical research director of Arthritis Research UK, Professor Alan Silman, said: “The possibility that omega-3 fatty acids could prevent osteoarthritis from developing has been a tantalising one. Some limited, previous research has suggested that we were a long way away from understanding the potential use in humans. However, this current research in guinea pigs is exciting as it brings us closer to understanding how omega-3 might fundamentally interfere with the osteoarthritis process, and that it could potentially be taken as a treatment.”

On the back of the results of his study, Dr Tarlton said that following government guidelines on dietary intake of omega-3 fatty acids could be effective in reducing the burden of osteoarthritis. Fish oil is far more effective than the flax oil based supplement, but for vegetarians flax oil remains a viable alternative.

“Most diets in the developed world are lacking in omega-3, with modern diets having up to 30 times too much omega-6 and too little omega-3. Taking omega-3 will help redress this imbalance and may positively contribute to a range of other health problems such as heart disease and colitis.”

Further studies are needed to determine the influence of omega-3 fatty acids on established disease in guinea pigs, and to confirm the effects in human osteoarthritis, said Dr Tarlton.

Osteoarthritis affects around eight million people in the UK, and is caused when the cartilage at the ends of bones wears away and the underlying bone thickens, leading to stiff, painful joints. Currently, there is no effective treatment to slow down disease progression, and treatment is limited to pain relief and ultimately joint replacement.

Paper: Regulation of osteoarthritis by omega-3 (n-3) polyunsaturated fatty acids in a naturally occurring model of disease, L. Knott, N.C. Avery, A.P. Hollander, J.F. Tarlton.  Osteoarthritis and Cartilage, Volume 19, Issue 9, September 2011.

Omega-3 fatty acid EPA cognitive decline: modulation by ApoEε4 allele and depression.

Sunday, October 16th, 2011

8.
Omega-3 fatty acids and cognitive decline: modulation by ApoEε4 allele and depression.
Samieri C, Féart C, Proust-Lima C, Peuchant E, Dartigues JF, Amieva H, Barberger-Gateau P.
Source

INSERM, U897, Department of Nutritional Epidemiology, Bordeaux, F-33076, France; University Victor Segalen Bordeaux 2, ISPED, 146 Rue Léo Saignat, Bordeaux, 33076, France.
Abstract

Long-chain omega-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) may slow cognitive decline. The ε4 allele of the ApolipoproteinE (ApoE), the main genetic risk factor for Alzheimer’s disease, and depressive symptoms, which are frequently associated with cognitive impairment in older persons, may modify this relationship. We estimated the associations between EPA and DHA plasma levels and subsequent cognitive decline over 7 years, taking into account ApoE-ε4 status and depressive symptoms, in a prospective population-based cohort. Participants (≥ 65 years, n = 1,228 nondemented at baseline) were evaluated at least once over three follow-up visits using four cognitive tests. Plasma EPA was associated with slower decline on Benton Visual Retention Test (BVRT) performances in ApoE-ε4 carriers, or in subjects with high depressive symptoms at baseline. Plasma DHA was associated with slower decline on BVRT performances in ApoE-ε4 carriers only. EPA and DHA may contribute to delaying decline in visual working memory in ApoE-ε4 carriers. In older depressed subjects, EPA, but not DHA, may slow cognitive decline.

Omega 3 Essential Fatty Acids are essential for optimal brain function

Saturday, October 8th, 2011

Omega 3 Essential Fatty Acids are essential for optimal brain function .During times of stress these essential nutrients are even more critical , the body cannot manufacture these nutrients themselves so they have to be provided by diet . The best sources of omega 3 essential fatty acids are those from oily fish such as sardines , anchovies , mackerel , salmon or you can take an omega 3 supplement – you should look for one that is both high concentration about 80% is preferred and high in active ingredient EPA . Unfortunately the majority of omega 3 products available to the consumer tend to be low concentration and low in EPA .
Research is now showing that deficiencies in these brain critical nutrients may manifest in mental health disorders such as major depression , suicidal tendancies , psychiatric disorders , developmental problems and impulsive violence. As well as that there are possible links re low omega 3 consumption and the increase in neurodegenerative disorders . Omega 3 fatty acids such eicosapentaenoic acid (EPA and docosahexaenoic (DHA) in particular are involved in many neuronal functions , Due to the reduction of omega 3 in todays modern diet there is more and more research being carried out re the benefits of omega3 especially EPA on the brain. The modern diet has a high ratio of omega 6 and a low ratio of omega 3 . Omega3 especially EPA is believed to be critical with regards the myelin sheaths ,Myelin is an insulating layer that forms around nerves, including those in the brain and spinal cord. It is made up of protein and fatty substances.
The purpose of the myelin sheath is to allow impulses to transmit quickly and efficiently along the nerve cells. If myelin is damaged, the impulses slow down.It is believed the omega3 active ingredients ie EPA not only acts as an anti inflammatory but also helps repair damage to the brain by promoting neuronal growth.

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

Depression is one of the first signs of Parkinson’s disease and is also one of the most overlooked

Friday, October 7th, 2011

Parkinson’s disease is a chronic disorder that worsens over time and results in the loss of brain cells that produce dopamine, a chemical messenger that controls movement. Parkinson’s disease usually affects people over age 50. The main symptoms of Parkinson’s disease are:

Tremor, or shaking, in the hands, arms, legs, jaw, and face
Rigidity, or stiffness, of the arms, legs, and torso
Slowness of movement
Impaired balance and coordination.

Currently the disease is believed to affect around 120,000 people in the UK and, with no cure, available treatments are aimed primarily at helping to control symptoms.

For people with Parkinson’s disease depression is common and disabling. It is also the most overlooked symptom and resulting condition of the disease. Whereas most people with Parkinson’s feel down and sad at one time or another, up to 60% of patients experience clinical depression.
Parkinson’s can also affect thinking and emotions. At present, there is no way to predict or prevent Parkinson’s disease One recent brain imaging study also suggeststhat people with Parkinson’s disease may have an unusually high number of reuptake pumps for the brain chemical messenger serotonin. Serotonin helps regulate mood, but overactive pumps reduce serotonin levels, possibly leading to depressive symptoms in some people with Parkinson’s disease.

Depression has been shown to be more common in people with Parkinson’s disease than in other chronic illnesses.Although feeling sad and “blue” after diagnosis of a chronic illness is part of the process, depression is more than just sadness. And in the case of Parkinson’s it is part of the illness, not simply a reaction to it.

Omega 3 EPA is as effective as Prozac in the treatment of medium to severe depression as well as that recent research has shown the potential benefits of EPA with regards Parkinsons Disease EPA is the most  potent  natural anti-inflammatory, and, unlike DHA, can directly inhibit the production of inflammatory products from the omega-6 arachidonic acid, which themselves are known to contribute to the progression of Parkinson’s vidence suggests an important role for omega−3 and omega−6 polyunsaturated fatty acids in the pathology and therapy of Parkinson’s disease and other neurodegenerative disorders, such as Alzheimer’s disease and Huntington’s chorea. However, because of the high concentration of polyunsaturated fatty acids in the brain, reactive products of lipid peroxidation are likely contributors to neurodegeneration. Increased intake of omega−6 fatty acids are known to increase risk of inflammatory disorders whilst, in contrast, the protective effects of omega−3 EPA and DHA supplementation have been demonstrated in experimental animal models of Parkinson’s disease

Parkinson’s disease (PD) is a neurodegenerative disorder, characterized by hypokinesia, but also mood and cognitive disorders. Neuropathologically, PD involves loss of nigrostriatal dopamine (DA) and secondary non-dopaminergic abnormalities. Inflammation may contribute to PD pathogenesis, evident by increased production of pro-inflammatory cytokines. PD onset has been positively associated with dietary intake of omega-(n)-6 polyunsaturated fatty acids (PUFA). On the other hand, omega-(n)-3 PUFA may benefit PD. One of these n-3 PUFA, eicosapentaenoic acid (EPA), is a neuroprotective lipid with anti-inflammatory properties, but its neuroprotective effects in PD are unknown. Thus, we presently tested the hypothesis that EPA can protect against behavioral impairments, neurodegeneration and inflammation in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-probenecid (MPTP-P) mouse model of PD. MPTP-P injections caused hypokinesia in the rotorod and pole test, hyperactivity in the open field, and impaired mice on the cued version (procedural memory) of the Morris water maze. MPTP-P caused a loss of nigrostriatal DA and altered neurochemistry in the frontal cortex and hippocampus. Furthermore, striatal levels of pro-inflammatory cytokines were increased, while the brain n-3/n-6 lipid profile remained unaltered. Feeding mice a 0.8% ethyl-eicosapentaenoate (E-EPA) diet prior to MPTP-P injections increased brain EPA and docosapentaenoic acid (DPA) but not docosahexaenoic acid (DHA) or n-6 PUFA. The diet attenuated the hypokinesia induced by MPTP-P and ameliorated the procedural memory deficit. E-EPA also suppressed the production of pro-inflammatory cytokines. However, E-EPA did not prevent nigrostriatal DA loss. Based on this partial protective effect of E-EPA, further testing may be warranted.

Parkinsons Disease treatment – Omega 3 EPA attenuates motor impairments and inflammation in the MPTP-probenecid mouse model of Parkinson’s disease.

Friday, October 7th, 2011

Ethyl-eicosapentaenoate (E-EPA) attenuates motor impairments and inflammation in the MPTP-probenecid mouse model of Parkinson’s disease.

Parkinson’s disease (PD) is a neurodegenerative disorder, characterized by hypokinesia, but also mood and cognitive disorders. Neuropathologically, PD involves loss of nigrostriatal dopamine (DA) and secondary non-dopaminergic abnormalities. Inflammation may contribute to PD pathogenesis, evident by increased production of pro-inflammatory cytokines. PD onset has been positively associated with dietary intake of omega-(n)-6 polyunsaturated fatty acids (PUFA). On the other hand, omega-(n)-3 PUFA may benefit PD. One of these n-3 PUFA, eicosapentaenoic acid (EPA), is a neuroprotective lipid with anti-inflammatory properties, but its neuroprotective effects in PD are unknown. Thus, we presently tested the hypothesis that EPA can protect against behavioral impairments, neurodegeneration and inflammation in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-probenecid (MPTP-P) mouse model of PD. MPTP-P injections caused hypokinesia in the rotorod and pole test, hyperactivity in the open field, and impaired mice on the cued version (procedural memory) of the Morris water maze. MPTP-P caused a loss of nigrostriatal DA and altered neurochemistry in the frontal cortex and hippocampus. Furthermore, striatal levels of pro-inflammatory cytokines were increased, while the brain n-3/n-6 lipid profile remained unaltered. Feeding mice a 0.8% ethyl-eicosapentaenoate (E-EPA) diet prior to MPTP-P injections increased brain EPA and docosapentaenoic acid (DPA) but not docosahexaenoic acid (DHA) or n-6 PUFA. The diet attenuated the hypokinesia induced by MPTP-P and ameliorated the procedural memory deficit. E-EPA also suppressed the production of pro-inflammatory cytokines. However, E-EPA did not prevent nigrostriatal DA loss. Based on this partial protective effect of E-EPA, further testing may be warranted.


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