I read the report on sciencedaily.com.  Notice how the "researchers"
criticize "antioxidant supplements" but then suggest an old, dangerous
drug (see the work of Thomas J. Moore) due to its antioxidant
properties.  This is the general state of "science" today in medicine
and nutrition.  As I've posted here many times before (starting a
couple of years ago), there is no such thing as "vitamin E."  Instead,
there are several different molecules with different effects on the
body.  Too much of one kind lowers the levels of one or more of the
others, and is actually dangerous, not healthy.  This is now
well-known, though not necessarily by these geniuses.  Do not take
alpha tocopherol by itself.  I think the Life Extension Institute makes
a good mixed tocopherol suspplement, but the best thing to do is to
just avoid foods that cause oxidative stress, meaning unsaturated fatty
acids (except in trace amounts) and oxidized cholesterol.  You can eat
berries and dark chocolate as well.  No need to spend extra money on
drugs or supplements, except for specific deficiency syndromes.

For example:

Despite the numerous antioxidant and anti-inflammatory properties of
alpha-tocopherol, results of large clinical trials assessing vitamin E
efficacy in heart disease have been disappointing. We know that
oxidative stress and inflammation play pivotal roles in heart disease.
Recent clinical trials even suggest that markers of inflammation, such
as C-reactive protein, may be better indicators of heart disease risk
than the old standby, cholesterol. So many scientists are asking, why
didn't vitamin E work?

It is surprising that alpha-tocopherol wasn't effective in the clinical
trials because it appears to have potent effects on cellular functions
that may modulate heart attack risk. Alpha-tocopherol can modulate the
inflammatory responses in white blood cells. It also can decrease blood
clotting by platelets-an important reason to let your physician know
that you are taking vitamin E. Another key function regulated by
alpha-tocopherol is vascular tone. Normal vascular function requires
responsiveness to nitric oxide (NO). Alpha-tocopherol not only mediates
NO production, but alpha-tocopherol supplementation in
hypercholesterolemic patients and in smokers maintains normal artery
wall flexibility. In clinical trials, vitamin C has also been found to
exert vasodilatory effects, probably through a different mechanism.

Unfortunately, most of the studies designed to demonstrate specific
alpha-tocopherol functions have been test-tube studies or are a result
of ex vivo treatment, i.e., plasma removed from subjects. Very few
measurements have been carried out in supplemented humans. Moreover,
all of the intervention studies evaluating the role of vitamin E in
heart disease were carried out using supplements containing
alpha-tocopherol. This has led to the concept that only
alpha-tocopherol has been well studied and that other members of the
vitamin E family, including gamma-tocopherol, have been neglected. But
that is not true.

It is well known that alpha-tocopherol supplements decrease plasma
gamma-tocopherol concentrations. What is less well appreciated is that
the body intentionally retains alpha-tocopherol. A special protein in
the liver, the alpha-tocopherol transfer protein, preferentially
maintains blood levels of alpha-tocopherol by incorporating only
alpha-tocopherol into low-density lipoprotein (LDL) for tissue
distribution. Our studies, currently in progress, show that the body
retains alpha-tocopherol three times longer than gamma-tocopherol.

Mechanisms of gamma-tocopherol action

Very few studies have evaluated gamma-tocopherol in the body, but those
that have suggest that it may have potentphysiological actions. While
both alpha- and gamma-tocopherol are potent antioxidants,
gamma-tocopherol has a unique function. Because of its different
chemical structure, gamma-tocopherol scavenges reactive nitrogen
species, which, like reactive oxygen species, can damage proteins,
lipids, and DNA. 5-Nitro-gamma-tocopherol, which is formed from these
scavenging reactions, may be a useful in vivo marker for estimating the
physiological relevance of such reactions. My laboratory has just
developed methods for measuring this marker, and we plan to use these
to assess gamma-tocopherol activity in humans under various kinds of
oxidative and inflammatory stress.

The RDA is only for alpha-tocopherol

The recommended dietary allowance (RDA) for vitamin E was set in 2000
as 15 mg of alpha-tocopherol per day. A diet rich in fruits and
vegetables and low in fat probably contains less than 15 mg of
alpha-tocopherol. Moreover, dietary alpha-tocopherol has probably
decreased over the past 50 years, not by losses in food processing, but
because of changes in recipes! Responding to concerns about the
relationship between certain dietary fats and heart disease, food
manufacturers have increased the vegetable oil content of processed
foods. Vegetable oils rich in polyunsaturated fats from, for example,
corn and soybeans, are also rich in gamma-tocopherol. Consuming these
oils as the major source of fat in the diet increases gamma-tocopherol
intakes to as much as 50 to 100 mg per day.

Gamma-tocopherol concentrations in the blood have been reported to be
significantly lower in coronary heart disease (CHD) patients compared
to healthy subjects, suggesting that the low Gamma-tocopherol
concentrations increased the risk of CHD. But Gamma-tocopherol may
simply be an indicator that the patients did not eat a diet low in
saturated fat and high in polyunsaturated fat. Higher vegetable oil
intakes in healthy subjects may have raised Gamma-tocopherol
concentrations. Although the beneficial effect may have been due to the
intake of polyunsaturated fat, Gamma-tocopherol itself may have some
benefit.

Prior to 2000, the RDA was expressed in "alpha-tocopherol
equivalents,"and Gamma-tocopherol was estimated to have 10% of the
activity of alpha-tocopherol. In contrast, the 2000 RDA defines that
the vitamin E requirement can only be met by alpha-tocopherol and
further specifies that the activity of synthetic (dl) alpha-tocopherol
is half that of natural (d) alpha-tocopherol. Thus, the 2000 RDA for
vitamin E is not based on antioxidant activities of the various dietary
forms of vitamin E (tocopherols and tocotrienols), but rather on the
observation that alpha-tocopherol is maintained in the circulation and
therefore must be required for some specific, as yet undefined,
function.

Key to establishing human vitamin E requirements is the identification
of alpha-tocopherol function. An important functional role of
alpha-tocopherol in human nutrition as an antioxidant is difficult to
justify because there are a variety of dietary antioxidants that are
more potent than alpha-tocopherol. However, only alpha-tocopherol has a
protein that regulates its plasma concentrations. This observation
argues for a unique and important physiological role for
alpha-tocopherol. The goal of the Traber lab is to discover that
function!

By:
Maret G. Traber, Ph.D.
Professor of Nutrition
LPI Principal Investigator

Source:
http://lpi.oregonstate.edu/ss03/vitamine.html