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Archive for May, 2015

Scientists Now Identify A Previously Unknown Function of Vitamin E

To reduce signs of aging, people massage Vitamin E into the skin and athletes consume it to improve endurance. Now, scientists have the evidence of one of vitamin E’s previously unknown body functions.

This powerful antioxidant vitamin helps repair tears in the plasma membranes that protect cells from outside forces and screen what enters and exits. Georgia Health Sciences University researchers reported their findings in the journal Nature Communications.

Everyday activities such as eating and exercise can tear the plasma membrane and the new research shows that vitamin E is essential to repair it. Without the proper repair of muscle cells, such as when muscles eventually waste away and die in a process similar to what
occurs in muscular dystrophy. Another example is the muscle weakness and common complaint from people with diabetes, the condition is associated with inadequate plasma membrane repair.

Century-old laboratory studies linked vitamin E deficiency to muscle problems but how that occurs remained a mystery until now. A  lack of membrane repair caused muscle wasting and death, which promptedthe researchers to look at vitamin E.

Vitamin E appears to assist repair in several ways. As an antioxidant, it helps eliminate destructive by-products from the body’s use of oxygen that impede repair. Because it’s lipid-soluble, vitamin E can actually insert itself into the membrane to prevent free radicals from attacking. It also can help keep important phospholipids, a major membrane component, compliant so they can better repair after a tear.

As a common example…  Exercise causes the cell powerhouse, the mitochondria, to burn a lot more oxygen than normal. “As an unavoidable consequence you produce reactive oxygen species,” the researchers explained.  The physical force of exercise actually tears the membrane. Vitamin E enables adequate plasma membrane repair despite the oxidant challenge and keeps the situation in balance.

When he mimicked what happens with exercise by using hydrogen peroxide to produce free radicals, he found that tears in skeletal muscle cells would not heal unless pretreated with vitamin E.
The next studies will be aided by two recent National Institutes of  Health grants, will include examining membrane repair in vitamin E-deficient animals.

They also want to examine membrane repair failure in diabetes.  The team showed that cells taken from animal models of types 1 and 2 diabetes have faulty repair mechanisms. They discovered high glucose was a culprit by soaking cells in a high-glucose solution for eight to 12 weeks, during which time they developed a repair defect. It’s also well documented that reactive oxygen species levels are elevated in diabetes.

The Nature Communications paper showed that vitamin E treatment in an animal model of diabetes restored some membrane repair ability.
Also, an analogue of the most biologically active form of vitamin E significantly reversed membrane repair deficits caused by high glucose and increased cell survival after tearing cells in culture.

Story Source: Georgia Health Sciences University.

Journal Reference:
Promotion of plasma membrane repair by vitamin E. Nature Communications, 2011;

Georgia Health Sciences University (2011, December 20). Scientists identify an innate function of vitamin E.

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Omega-3 Fatty Acids Prevent (or Slow) Progression of Osteoarthritis

Salmon Oil

New Research From University of Bristol UK Report… 
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 laboratory subjects, 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 from fish oil or flaxseed oil sources, may help to slow down the progression of osteoarthritis, or even prevent it occurring, confirming reports about the benefits of fish oil for joint health.

Researchers 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,” they said.

They added “and all of the evidence supports the use of omega-3 in human disease.”

Medical researchers of Arthritis Research UK said: “The possibility that omega-3 fatty acids could prevent osteoarthritis from developing has been a tantalising one. Some limited, previous research in dogs 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.”

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 the researchers.

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.

Story Source: University of Bristol.

Journal Reference: “Regulation of osteoarthritis by omega-3 (n-3) polyunsaturated fatty acids in a naturally occurring model of disease. Osteoarthritis and Cartilage”  2011;

This article is for informational and educational purposes only, and is not intended to provide medical advice, diagnosis or treatment. Contact your doctor or healthcare professional for medical and nutritional consultation.

Dietary Iron Intake During Teenage Years Crucial for Brain Functioning in Later Life

Important new findings appear in  the journal Proceedings of the National Academy
of Sciences

Doctors often prescribe Iron for medical reasons and it’s typically available over the counter as a
dietary supplement. Although it’s known that too little iron can result in cognitive problems, it’s also
known that too much promotes neurodegenerative diseases.

Researcher scientists at UCLA have now found that in addition to causing cognitive problems, a lack of iron early in life can affect the brain’s physical structure as well.

The UCLA neurology research team examined levels of transferrin, a protein that transports iron throughout the body and brain, in adolescents and discovered that the transferrin levels were related to measurable differences in both the brain’s macro-structure and micro-structure when the adolescents reached young adulthood.

The researchers also identified a common set of genes that influences both transferrin levels and brain structure. The new discovery may shed light on the neural mechanisms by which iron affects cognition, neuro-development and neuro-degeneration, they said.Their findings appear in the current online edition of the journal “Proceedings of the National Academy of Sciences”

Iron and the proteins that transport it are critically important for brain function. Iron deficiency is the most common nutritional deficiency worldwide, causing poor cognitive achievement in school-aged children. Yet later in life, iron overload is associated with damage to the brain, and abnormally high iron concentrations have been found in the brains of patients with Alzheimer’s, Parkinson’s and Huntington diseases.

Since both a deficiency and an excess of iron can negatively impact brain function, the body’s regulation of iron transport to the brain is crucial. When iron levels are low, the liver produces more transferrin for increased iron transport. The researchers wanted to know whether brain structure in healthy adults was also dependent on transferrin levels.

“We found that healthy brain wiring in adults depended on having good iron levels in your teenage years,” the researchers explained. “This connection was a lot stronger than we expected, especially as we were looking at people who were young and healthy” they said.

To assess brain volume and integrity, the team collected brain MRI scans on 615 healthy young-adult twins and siblings, who had an average age of 23. 574 were also scanned with an MRI called a “diffusion scan,” which maps the brain’s myelin connections and their strength, or integrity. Myelin is the fatty sheath that coats the brain’s nerve axons, allowing for efficient conduction of nerve impulses, and iron plays a key role in myelin production.

Previously researchers used studies to determine whether iron availability in the during period of adolescence impacted the organization of the brain later in life. This period of life is developmentally crucial.

“Adolescence is a period of high vulnerability to brain insults, and the brain is still very actively developing,” they emphasised.

By averaging the subjects’ transferrin levels, which had been assessed repeatedly at 12, 14 and 16 years of age, the researchers estimated iron availability to the brain during adolescence.

The team discovered that subjects who had elevated transferrin levels (a common indication of poor iron levels in a person’s diet) had structural changes in brain regions that are vulnerable to neurodegeneration. Interestingly, further analyses of the twins in the study revealed that a common set of genes influences both transferrin levels and brain structure.

One of the genetic links, a specific variation in a gene called HFE, which is known to influence blood transferrin levels, was associated with reduced brain-fiber integrity, although subjects carrying this gene variant did not yet show any symptoms of disease or cognitive impairment.

“So this is one of the deep secrets of the brain,” they said. “the iron in our diet affects the brain so much in our teen years. It matters very much.because myelin speeds your brain’s communications, and iron is vital for making myelin, poor iron levels in childhood erode your brain reserves which you need later in life to protect against aging and Alzheimer’s.

“It underscores the need for a balanced diet in the teenage years, when your brain’s command center is still actively maturing. ”

The findings may aid future studies of how iron transport affects brain function, development and the risk of neurodegeneration.

The research was supported by the National Institute of Child Health and Human Development; Australia’s National Health and Medical Research Council; the Achievement Rewards for College Scientists Foundation; the National Institute of Mental Health; and the Australian Research Council Future Fellowship.

Story Source: University of California – Los Angeles.

Journal Reference:
PNAS Plus: Brain structure in healthy adults is related to serum transferrin and the H63D polymorphism in the HFE gene. Proceedings of the National Academy of Sciences, 2012;

This article is for informational and educational purposes only;
It is not intended to provide medical advice, diagnosis or treatment. Contact your doctor or healthcare professional for medical and nutritional consultation.

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