Posts tagged fatty acids
Articles and news from the latest research reports.
Low Omega-3 could explain why some children struggle with reading
An Oxford University study has shown that a representative sample of UK schoolchildren aged seven to nine years had low levels of key Omega-3 fatty acids in their blood. Furthermore, the study found that children’s blood levels of the long-chain Omega-3 DHA (the form found in most abundance in the brain) ‘significantly predicted’ how well they were able to concentrate and learn. Oxford University researchers explained the findings, recently published in the journal PLOS ONE, at a conference in London on 4 September.
The study was presented at the conference by co-authors Dr Alex Richardson and Professor Paul Montgomery from Oxford University’s Centre for Evidence-Based Intervention in the Department of Social Policy and Intervention. It is one of the first to evaluate blood Omega-3 levels in UK schoolchildren. The long-chain Omega-3 fats (EPA and DHA) found in fish, seafood and some algae, are essential for the brain’s structure and function as well as for maintaining a healthy heart and immune system. Parents also reported on their child’s diet, revealing to the researchers that almost nine out of ten children in the sample ate fish less than twice a week, and nearly one in ten never ate fish at all. The government’s guidelines for a healthy diet recommend at least two portions of fish a week. This is because like vitamins, omega-3 fats have to come from our diets – and although humans can in theory make some EPA and DHA from shorter-chain omega-3 (found in some vegetable oils), research has shown this conversion is not reliable, particularly for DHA, say the researchers.
Blood samples were taken from 493 schoolchildren, aged between seven and nine years, from 74 mainstream schools in Oxfordshire. All of the children were thought to have below-average reading skills, based on national assessments at the age of seven or their teachers’ current judgements. Analyses of their blood samples showed that, on average, just under two per cent of the children’s total blood fatty acids were Omega-3 DHA (Docosahexaenoic acid) and 0.5 per cent were Omega-3 EPA (Eicosapentaenoic acid), with a total of 2.45 per cent for these long-chain Omega-3 combined. This is below the minimum of 4 per cent recommended by leading scientists to maintain cardiovascular health in adults, with 8-12 per cent regarded as optimal for a healthy heart, the researchers reported.
Co-author Professor Paul Montgomery said: ‘From a sample of nearly 500 schoolchildren, we found that levels of Omega-3 fatty acids in the blood significantly predicted a child’s behaviour and ability to learn. Higher levels of Omega-3 in the blood, and DHA in particular, were associated with better reading and memory, as well as with fewer behaviour problems as rated by parents and teachers. These results are particularly noteworthy given that we had a restricted range of scores, especially with respect to blood DHA but also for reading ability, as around two-thirds of these children were still reading below their age-level when we assessed them. Although further research is needed, we think it is likely that these findings could be applied generally to schoolchildren throughout the UK.’
Co-author Dr Alex Richardson added: ‘The longer term health implications of such low blood Omega-3 levels in children obviously can’t be known. But this study suggests that many, if not most UK children, probably aren’t getting enough of the long-chain Omega-3 we all need for a healthy brain, heart and immune system. That gives serious cause for concern because we found that lower blood DHA was linked with poorer behaviour and learning in these children.
‘Most of the children we studied had blood levels of long-chain Omega-3 that in adults would indicate a high risk of heart disease. This was consistent with their parents’ reports that most of them failed to meet current dietary guidelines for fish and seafood intake. Similarly, few took supplements or foods fortified with these Omega-3.’
The current findings build on earlier work by the same researchers, showing that dietary supplementation with Omega-3 DHA improved both reading progress and behaviour in children from the general school population who were behind on their reading. Their previous research has already shown benefits of supplementation with long-chain omega-3 (EPA+DHA) for children with ADHD, Dyspraxia, Dyslexia, and related conditions. The DHA Oxford Learning and Behaviour (DOLAB) Studies have now extended these findings to children from the general school population.
‘Technical advances in recent years have enabled the measurement of individual Omega-3 and other fatty acids from fingerstick blood samples. ‘These new techniques have been revolutionary – because in the past, blood samples from a vein were needed for assessing fatty acids, and that has seriously restricted research into the blood Omega-3 status of healthy UK children until now,’ said Dr Richardson.
(Source: ox.ac.uk)
Diabetes drug shows promise in treatment of neurodegenerative disease
Researchers in Spain have found that a drug used to control Type II diabetes can help repair the spinal cords of mice suffering from the inherited disease adrenoleukodystrophy which, untreated, leads eventually to a paralysis, a vegetative state and death. They believe that their findings may be relevant to other neurodegenerative diseases. A Phase II trial will be starting shortly. The research is published simultaneously on line in the journal Brain.
A drug used to control Type II diabetes can help repair the spinal cords of mice suffering from the inherited disease adrenoleukodystrophy which, untreated, leads eventually to a paralysis, a vegetative state and death. This is an important step along the road to the development of a therapy for the human disease for which current treatment options are scarce and only partially effective, the annual conference of the European Society of Human Genetics will hear tomorrow (Sunday).
Professor Aurora Pujol, a research professor for the Catalan Government Research Body ICREA, working as Director of the Neurometabolic Diseases Laboratory at IDIBELL, Barcelona, Spain, investigated the role of mitochondria, the power plant of the cell, in adrenoleukodystrophy, a disease caused by the inactivation of the ABCD1 transporter of fatty acids in peroxisomes. This inactivation leads to the accumulation of fatty acids in organs and blood plasma, and causes spinal cord degeneration.
“ABCD1 is a protein located in the peroxisomes, compartments of the cell that detoxify chemicals and lipids, and thus the implication of mitochondria in such a disease was not obvious. But we knew from recent research that oxidative stress – where there is increased production of chemically active oxygen-containing molecules, and also significant decrease in the effectiveness of the body’s antioxidant defences – was involved. We also knew that bioenergetic failure appeared before disease symptoms. We therefore decided to investigate the role of the mitochondria”, Professor Pujol will say.
The group of diseases known as leukodystrophies are characterised by progressive loss of the myelin sheath, the fatty covering that acts as an insulator around nerve fibres. Damage to the myelin sheath impairs the conduction of signals in the affected nerves and leads to locomotor problems.
“We knew that early oxidative damage and bioenergetic dysfunction underlay the late onset degeneration of nerve fibres observed in the mouse model of X-linked adrenoleukodystrophy (X-ALD), the most frequently inherited leukodystrophy, so we looked at mitochondria for further clues. We found that the X-ALD mice showed a loss of mitochondria at 12 months of age, prior to disease symptoms, so this could not be a consequence of the disease, but rather a contributing factor. We also knew that the pathway involved in the mitochondrial loss could be treated by the use of the diabetes drug pioglitazone, so we decided to test its effect in the mice”, Professor Pujol will say.
Pioglitazone halted the nerve fibre degeneration by preventing the loss of mitochondria, and inhibiting metabolic failure and oxidative stress in the treated mice, and hence also halted locomotor disabilities. The researchers were able to prove this both through analysis of spinal cords post mortem, and in vivo by putting the mice through a number of physical tests.
Although X-ALD is a relatively rare disease with a minimum incidence of 1 in 17 000 males, there are other neurodegenerative disorders caused by myelin sheath degeneration, for example multiple sclerosis, and many others where impaired bioenergetics combined with oxidative stress and degeneration of axons are known to be involved. The latter category of disease includes Parkinson’s, Huntington’s, and Alzheimer’s. “It is possible that our findings may be relevant to these conditions as well,” says Professor Pujol.
“Following on from these promising results, together with Professor Patrick Aubourg from the Hôpital Bicêtre, Paris, we will shortly be starting a multi-centre phase II clinical trial of pioglitazone in adult patients suffering from a late onset variant of adrenoleukodystrophy. Our research has shown that it will be feasible to monitor the biological effects of the drug by looking for biomarkers of oxidative damage in blood cells or plasma. We are happy to have made a contribution to finding a simple and effective treatment to a group of devastating diseases”, she will conclude.
(Source: alphagalileo.org)
Study of the machinery of cells reveals clues to neurological disorder
Investigation by researchers from the University of Exeter and ETH Zurich has shed new light on a protein which is linked to a common neurological disorder called Charcot-Marie-Tooth disease.
Peroxisomes (green) and mitochondria (red) in a mammalian cell. The nucleus (blue) contains the cellular DNA.
The team has discovered that a protein previously identified on mitochondria - the energy factories of the cell - is also found on the fat-metabolising organelles peroxisomes, suggesting a closer link between the two organelles.
Charcot-Marie-Tooth disease is currently incurable and affects around one in every 2,500 people in the UK, meaning that it is one of the most common inherited neurological disorders, thus understanding the molecular basis of the disease is of great importance. Symptoms can range from tremors and loss of touch sensation in the feet and legs to difficulties with breathing, swallowing, speaking, hearing and vision.
The research published online in EMBO Reports combines work from University of Exeter Biosciences researcher Dr Michael Schrader and PhD student Sofia Guimaraes. The major finding of the study is that the protein GDAP1, originally thought to only be involved in fragmentation of mitochondria, also contributes to the regulation of peroxisome number through their division.
Peroxisomes are small organelles occurring in nearly all cells, from yeast to crop plants to humans, and are essential for cell viability due to their important role in the metabolism of fatty acids and reactive oxygen species. Peroxisomes are also of particular interest as they play a key role in ageing.
This current study shows that the division of both mitochondria and peroxisomes follows a similar mechanism, although many of the disease-causing mutations occur in a region of the gene that is more critical for mitochondrial than peroxisomal division.
Dr Michael Schrader said of this project: “This study supports our hypothesis of a closer connection between mitochondria and peroxisomes. We have identified several membrane proteins, which are shared by both organelles, particularly key components of the division machinery, meaning there must be coordinated biogenesis and cross-talk.”
As numerous diseases have been linked to problems in the mitochondria, Dr Schrader proposes that this connection could have far-reaching medical implications.
This work contributes to the research being addressed through the prestigious Marie Curie Initial Training Network PERFUME programme (PERoxisome, FUnction, and MEtabolism), recently awarded to Michael Schrader along with several other top European research groups which focus on peroxisome biology.
(Source: exeter.ac.uk)
New clues to causes of peripheral nerve damage
Anyone whose hand or foot has “fallen asleep” has an idea of the numbness and tingling often experienced by people with peripheral nerve damage. The condition also can cause a range of other symptoms, including unrelenting pain, stinging, burning, itching and sensitivity to touch.
Although peripheral neuropathies afflict some 20 million Americans, their underlying causes are not completely understood. Much research has focused on the breakdown of cellular energy factories in nerve cells as a contributing factor.
Now, new research at Washington University School of Medicine in St. Louis points to a more central role in damage to energy factories in other cells: Schwann cells, which grow alongside neurons and enable nerve signals to travel from the spinal cord to the tips of the fingers and toes.
The finding may lead to new therapeutic strategies to more effectively treat symptoms of this highly variable disorder, the scientists report March 6 in the journal Neuron.
“We found that a toxic substance builds up in Schwann cells that have disabled energy factories, leading to the same kind of nerve damage seen in patients with neuropathies,” says senior author Jeffrey Milbrandt, MD, PhD, the James S. McDonnell Professor of Genetics and head of the Department of Genetics. “Now, we’re evaluating whether drugs can block the buildup of that toxin, which could lead to a new treatment for the condition.”
The most common cause of peripheral neuropathy is diabetes, which accounts for about half of all cases. The condition also can occur in cancer patients treated with chemotherapy, which can damage nerves.
In the body, Schwann cells wrap tightly around nerve axons, the fibers that relay nerve signals. Graduate student and first author Andreu Viader and colleagues in Milbrandt’s lab studied Schwann cells in mice with genetically disabled mitochondria, or cellular energy factories. Under normal conditions, these mitochondria produce fuel and intermediates of energy metabolism that allow nerve cells to function.
The researchers showed that the crippled mitochondria activated a stress response in the Schwann cells. Instead of synthesizing fatty acids, a key component of Schwann cells, the cells burned fatty acids for fuel.
Over time, inefficient burning of fatty acids by the crippled mitochondria leads to a build up of acylcarnitines, a toxic substance, in the Schwann cells. The researchers found levels of acylcarnitines up to 100-fold higher in these mutant Schwann cells than in healthy Schwann cells.
And the bad news doesn’t end there. Eventually, the toxin leaks out of the Schwann cells and onto the nerve axons. Studying neurons in petri dishes, the researchers showed that acylcarnitines damage nerve axons and disrupt the ability of nerves to relay signals.
“The toxin leaking out of the Schwann cells and onto the adjacent nerve axons causes damage that results in pain, numbness, tingling and other symptoms,” Milbrandt says. “We think that is a likely mechanism to explain the degeneration of axons that is known to occur in peripheral neuropathies.”
The new research suggests that drugs that inhibit the buildup of acylcarnitines may block axonal degeneration. Milbrandt and his team now are evaluating the drugs in mice with disabled Schwann cells to see if they can slow or alleviate the decay of axons.
Omega-3 Lipid Emulsions Markedly Protect Brain After Stroke in Mouse Study
Triglyceride lipid emulsions rich in an omega-3 fatty acid injected within a few hours of an ischemic stroke can decrease the amount of damaged brain tissue by 50 percent or more in mice, reports a new study by researchers at Columbia University Medical Center.
The results suggest that the emulsions may be able to reduce some of the long-term neurological and behavioral problems seen in human survivors of neonatal stroke and possibly of adult stroke, as well. The findings were published today in the journal PLoS One.
Currently, clot-busting tPA (recombinant tissue-type plasminogen activator) is the only treatment shown to improve recovery from ischemic stroke. If administered soon after stroke onset, the drug can restore blood flow to the brain but may not prevent injured, but potentially salvageable, neurons from dying.
Drugs with neuroprotective qualities that can prevent the death of brain cells damaged by stroke are needed, but even after 30 years of research and more than 1000 agents tested in animals, no neuroprotectant has been found effective in people.
Omega-3 fatty acids may have more potential as neuroprotectants because they affect multiple biochemical processes in the brain that are disturbed by stroke, said the study’s senior author, Richard Deckelbaum, MD, director of the Institute of Human Nutrition at Columbia’s College of Physicians & Surgeons. “The findings also may be applicable to other causes of ischemic brain injury in newborns and adults,” added co-investigator Vadim S. Ten, MD, PhD, an associate professor of pediatrics from the Department of Pediatrics at Columbia.
The effects of the omega-3 fatty acids include increasing the production of natural neuroprotectants in the brain, reducing inflammation and cell death, and activating genes that may protect brain cells. Omega-3 fatty acids also markedly reduce the release of harmful oxidants into the brain after stroke. “In most clinical trials in the past, the compounds tested affected only one pathway. Omega-3 fatty acids, in contrast, are very bioactive molecules that target multiple mechanisms involved in brain death after stroke,” Dr. Deckelbaum said.
The study revealed that an emulsion containing only DHA (docosahexaenoic acid), but not EPA (eicosapentaenoic acid), in a triglyceride molecule reduced the area of dead brain tissue by about 50 percent or more even when administered up to two hours after the stroke. Dr. Deckelbaum noted, “Since mice have a much faster metabolism than humans, longer windows of time for therapeutic effect after stroke are likely in humans.” Eight weeks after the stroke, much of the “saved” mouse brain tissue was still healthy, and no toxic effects were detected.
(Image: Shutterstock)
Vitamin D, omega-3 may help clear amyloid plaques found in Alzheimer’s
A team of academic researchers has pinpointed how vitamin D3 and omega-3 fatty acids may enhance the immune system’s ability to clear the brain of amyloid plaques, one of the hallmarks of Alzheimer’s disease.
In a small pilot study published in the Feb. 5 issue of the Journal of Alzheimer’s Disease, the scientists identified key genes and signaling networks regulated by vitamin D3 and the omega-3 fatty acid DHA (docosahexaenoic acid) that may help control inflammation and improve plaque clearance.
Previous laboratory work by the team helped clarify key mechanisms involved in helping vitamin D3 clear amyloid-beta, the abnormal protein found in the plaque. The new study extends the previous findings with vitamin D3 and highlights the role of omega-3 DHA.
"Our new study sheds further light on a possible role for nutritional substances such as vitamin D3 and omega-3 in boosting immunity to help fight Alzheimer’s," said study author Dr. Milan Fiala, a researcher at the David Geffen School of Medicine at UCLA.
Discovery offers new treatment for epilepsy
New drugs derived from components of a specific diet used by children with severe, drug-resistant epilepsy could offer a new treatment, according to research published today in the journal Neuropharmacology.
Scientists from Royal Holloway, in collaboration with University College London, have identified specific fatty acids that have potent antiepileptic effects, which could help control seizures in children and adults.
The discovery could lead to the replacement of the ketogenic diet, which is often prescribed for children with severe drug-resistant epilepsy. The high fat, low carbohydrate diet is thought to mimic aspects of starvation by forcing the body to burn fats rather than carbohydrates. Although often effective, the diet has attracted criticism, as side effects can be significant and potentially lead to constipation, hypoglycaemia, retarded growth and bone fractures.
By pinpointing fatty acids in the ketogenic diet that are effective in controlling epilepsy, researchers hope that they can develop a pill for children and adults that could provide similar epilepsy control, but lacks the side effects of the diet.
Professor Robin Williams from the Centre of Biomedical Sciences at Royal Holloway said: “This is an important breakthrough. The family of medium chain fatty acids that we have identified provide an exciting new field of research with the potential of identifying, stronger, and safer epilepsy treatments.”
The study tested a range of fatty acids found in the ketogenic diet against an established epilepsy treatment. Researchers found that not only did some of the fatty acids outperform the drug in controlling seizures, they also had fewer side effects.
(Source: alphagalileo.org)