Two recent studies offer new evidence suggesting an alternative form
of natural vitamin E can be taken by mouth and will reach the blood in
humans at levels determined to protect against stroke and other
diseases.

Vitamin E occurs naturally in eight different forms. The primary
vitamin E on drugstore shelves is called tocopherol, or TCP. But
another natural form of vitamin E surfacing as a potent
neuroprotective agent in repeated Ohio State University Medical Center
studies is tocotrienol, or TCT.

This form, while not abundant in the American diet, occurs naturally
in palm oil; this vegetable oil is increasingly used in prepared foods
because it has no trans fat.

In the first study of this form of the nutritional supplement in
humans, Ohio State researchers determined that a moderate dose of
tocotrienol reached concentrations in human blood plasma that would be
more than adequate to protect against neurological damage that follows
stroke. These findings were published in the May issue of the journal
Antioxidants & Redox Signaling.

In a separate study, the scientists determined that TCT is effective
at two concentrations, one at which it functions as an antioxidant,
and another, lower concentration at which the supplement offers
non-antioxidant protection. Both functions of TCT are directed against
neurodegeneration. These findings were published June 26 in an online
edition of the Journal of Neurochemistry.

"We have determined that when administered orally, tocotrienol can
reach concentrations needed to serve these dual protective functions,"
said Chandan Sen, professor and vice chair of surgery, deputy director
of the Davis Heart and Lung Research Institute at OSU, and senior
author of both studies. "It is a regular dietary ingredient in Asia,
so it can safely be a part of a daily diet within prepared foods or as
a supplement in the United States . Can it be therapeutically used to
prevent stroke? Results from animal studies are encouraging, but it is
still too soon to tell for humans. More mechanistic and outcomes
studies are warranted."

In the first study, collaborating scientists at Wayne State University
fed participants 400 milligrams of a time-release formulation of a
supplement containing primarily TCT. Researchers collected blood
samples from the participants two, four, six and eight hours after
supplementation.

Sen said the maximum TCT concentrations in the bloodstream of
supplemented patients averaged concentrations between 12 and 30 times
higher than that needed to completely prevent stroke-related
neurodegeneration as determined by earlier research.

Conventional wisdom has suggested that TCT, if eaten, cannot be
carried to organs because the protein known as tocopherol transfer
protein (TTP), which delivers TCP throughout the body, doesn't
transport TCT very well.

"Our results demonstrate that TCT is efficiently delivered to the
bloodstream despite the fact that the transfer protein has a lower
affinity for TCT than it has for TCP," Sen said. Absorption of TCT is
increased when the supplement is taken with fat-containing food, so
the research participants took the study supplement with a high-fat
(60 grams) meal to increase the efficiency of absorption.

The findings corresponded closely with previous work as well as the
more recent study that sought to determine the levels at which TCT
functions as an antioxidant, an agent that protects cells against the
effects of free radicals. Free radicals are potentially damaging
by-products of energy metabolism that can damage cells and are
implicated in the development of cardiovascular disease and cancer.
The tocopherol, or most common, form of vitamin E is known for its
antioxidant properties.

In previous studies, the scientists found that moderate oral doses of
TCT before a stroke significantly reduced stroke injury in
hypertensive rats.

In the more recent study published in the Journal of Neurochemistry,
researchers observed the effects of TCT on neurological damage that
can be caused in two different ways: through the presence of
homocysteic acid, which in excess can cause vascular and neuronal
lesions associated with cardiovascular disease, and the fatty acid
linoleic acid, which can directly stimulate damaging free radical
activity. Fatty acids are related to stroke: They rapidly accumulate
when a clot in a vessel stops blood flow to the brain, and play a role
in irreversible brain injury.

To observe the TCT's effectiveness, rodent neural cells were
pretreated with extremely low concentrations of TCT; these cells
avoided the cell death associated with toxicity caused by homocysteic
acid. But to reduce free-radical activity and resulting neurotoxicity,
the scientists found that a higher concentration of TCT was needed:
Tocotrienol does not exhibit antioxidant properties until it reaches a
concentration 10 to 25 times stronger than the concentration that
prevented the cell death signal.

The National Institutes of Health supported this research. Ohio State
co-authors of the Journal of Neurochemistry study were Savita Khanna,
Sashwati Roy, Narasimham L. Parinandi and Mariah Maurer, all with the
Davis Heart and Lung Research Institute. Ohio State co-authors of the
Antioxidants & Redox Signaling paper were Viren Patel, Khanna and Roy,
all of the Laboratory of Molecular Medicine.

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