Vitamin E – After a Stroke
January 22, 2010
A stroke occurs when the blood supply to part of the brain is suddenly blocked by a blood clot or when a blood vessel in the brain bursts, driving blood into the spaces surrounding brain cells, or neurons. The result can be brain damage that leaves stroke survivors with disabilities ranging from one-sided paralysis or weakness to problems with thinking, attention, memory and learning. But new research by Ohio State University scientists set for publication in an upcoming edition of the Journal of Neurochemistry concludes a specific type of vitamin E known as tocotrienol (TCT) could prevent brain cells from dying after a stroke.
Tocopherols are the best-known form of vitamin E and the kind usually found in supplements. However, the vitamin occurs naturally in seven other different forms, including TCT. Although not widely found in the typical American diet, it is common in foods that comprise a typical Southeast Asian diet. Food sources of TCT include rice bran oil, barley, wheat germ and oats.
“Our research suggests that the different forms of natural vitamin E have distinct functions. The relatively poorly studied tocotrienol form of natural vitamin E targets specific pathways to protect against neural cell death and rescues the brain after stroke injury,” Chandan Sen, professor and vice chair for research in Ohio State’s Department of Surgery and senior author of the study, said in a statement to the media.
Over the past decade, the Ohio State University research team has studied how this form of vitamin E protects the brain in animal and cell models. But according to Dr. Sen, their new study provides specific details about how that protection works. Bottom line: they’ve identified an enzyme called cystolic calcium-dependent phospholipase A2 (cPLA2, for short) that tocotrienol targets to protect neurons after a stroke.
“We have studied an enzyme that is present all the time, but one that is activated after a stroke in a way that causes neurodegeneration. We found that it can be put in check by very low levels of tocotrienol,” Dr. Sen said. “So what we have here is a naturally derived nutrient, rather than a drug, that provides this beneficial impact.”
The researchers explained that the blocked blood flow to the brain associated with a stroke causes an excess of the neurotransmitter glutamate to be released. In normal amounts, glutamate is beneficial and important for memory and learning. But when produced in large amounts due to the brain trauma of a stroke, it triggers a cascade of reactions that leads to the death of neurons and causes the most serious stroke damage.
For their study, Dr. Sen and colleagues took cells from the hippocampus region of developing mouse brains and added excess glutamate to produce the type of changes seen in the brain after a stroke. In the presence of excess glutamate, the cPLA2 enzyme released a fatty acid called arachidonic acid which normally helps maintain the stability of health cell membranes. Under stroke conditions, however, with high levels of glutamate present, arachidonic acid undergoes an enzymatic chemical reaction that makes it toxic — then brain cells are poisoned and start to die.
But when the researchers added tocotrienol to the cells that had been exposed to excess glutamate, the vitamin E decreased the release of fatty acids by 60 percent when compared to cells exposed to glutamate alone. What’s more, the brain cells treated with the TCT form of vitamin E were about four times more likely to survive than brain cells exposed to glutamate alone.
In the press statement, Dr. Sen noted that the amount of TCT needed to achieve these brain cell protecting effects is quite small — a concentration about 10 times lower than the average amount of tocotrienol circulating in humans who consume this form of vitamin E regularly. The Ohio State University researchers intend to continue their research to see if TCT can successfully prevent and treat strokes in humans.
Editor’s note: NaturalNews is opposed to the use of animals in medical experiments that expose them to harm. We present these findings in protest of the way in which they were acquired.