Certainly the Shutes were proponents of vitamin E in all is
forms. They used very large doses in combination with
the Levine chair therapy. They were proponents of
of early ambulation of heart attack patients.
As I recall the standard of care in their day
was a months bed rest. The chair therapy involved
getting the patient in a position in which the legs
raised relative to the heart. They also have been
rather aggressive with the aspirin, but I reach on
this later point. While they advocated E as preventive,
they were using it in acute cases.

What has amused me through the years is that the Shutes
gave vitamin E with only the greatest care (low titrated dosed) in
congestive heart cases. And the opponents to the use
of vitamin E have referred to this view without
crediting the Shutes. Repeating the warning but
not citing the source. So it seems both
camps draw from the Shutes and forget them at
the same time.

At 6 ounces of wine with rice
and squash and pickled bell peppers
in the belly..........JQ

"Sbharris[atsign]ix.netcom.com" <sbharris[at]ix.netcom.com> wrote in message
news:1111004795.495107.195480[at]l41g2000cwc.googlegroups.com...
- quote -

Hi,

Sbharris[atsign]ix.netcom.com wrote:
- quote -

And in this study there was a 7% reduction in total mortality
despite the fact that the vit. E was given to a group in which 59% were
taking aspirin. As I've explained before both vit E and aspirin
antagonize vit K and BOTH independently cause blood thinning, internal
bleeding, and haemorrhagic stroke. The combination of the two together
in clinical trials always results in mildly unfavorable or null results
unless given with sufficient C (at least a two to one ratio) to swamp
the negative effects of the two ganging up on vit K, a vitamin of which
nearly everyone is deficient. Three trials of E alone have been done in
populations that don't take aspirin and all three showed benefits.
There is little or no inconsistency in the literature. Once more I will
spell it out for you.
Four trials of E with hi dose C-all favorable. These are the
only four.
Three trials of E without C or aspirin----- all favorable but
less so. I think these are the only ones. Can anyone prove me wrong?
Quite a few trials of E with people taking aspirin, or beta
carotene in smokers, or deprenyl (which is associated with excess
mortality in humans)-------UNfavorable.

This is the literature on the randomized, placebo controlled,
intervention trials of vit. E. This is the only place you will see it
properly summarized. I'm not too happy about supporting thousands of
clinical researchers with my tax dollars, and then having to do the
work myself. )



- quote -



Only in cohorts that are taking aspirin





- quote -


Maybe because they read direct evidence of this theoretically
plausible fact that I posted. I doubt that you will be able to post any
evidence that it doesn't. See my comments on PMID 12090883 in
sci.life-extension. For those that don't understand the significance
of hi odds ratios in epidemiology I posted a short essay a while back.


- quote -

I've given seven gold standard, intervention trials on vit E and C,
referenced in previous posts, showing excellent cardiovascular and
mortality benefits when taken properly. I've made several public
claims that there are no negative trials without contradiction. If
these were drugs they would get FDA approval and be widely accepted.
Millions of people are dying annually of cardiovascular disease. I have
just one question for the medical community.
WHUTSWRONGWITCHYOUGUYS????

Thomas

Show me the money. Give something that works and don't tell me why it
doesn't work.


"Juhana Harju" <shantigiri[at]despammed.com> wrote in message
news:39rnsjF64tcb5U1[at]individual.net...
- quote -

Totally agree with you on that one.
One important exception though and it is one important one.
If it works then it doesn't matter. It is important to be critical of
studies but it is hard to argue with success especially if it is proven over
and over again.
Even if the logic does not go along with why it works or why it shouldn't
work. You can't argue with success.


"Sbharris[atsign]ix.netcom.com" <sbharris[at]ix.netcom.com> wrote in message
news:1111004795.495107.195480[at]l41g2000cwc.googlegroups.com...
- quote -

Juhana Harju wrote:
:: Sbharris[atsign]ix.netcom.com wrote:
:::: Look, if this study had been done with dl-alpha, critics would be
:::: complaining it wasn't done with the ddd natural isomer. And since
:::: it was done with the d,d,d, now they're complaining it wasn't done
:::: with the proper "natural mix" of alpha, beta, gamma, and delta
:::: isomers (whatever *that* is-- since it varies widely within
:::: different foods and cultural food mixes, and the body can, and
:::: does, methylate the more common natural gamma to more-needed and
:::: protein carrier specific alpha). [...]
::
:: AFAIK, many, perhaps most health benefits of dietary vitamin E are
:: associated with gamma-tocopherol. Why do they keep doing studies with
:: supplemental alpha-tocopherol and even worse, dl-alpha? It makes me
:: suspect that they want to get negative results.

This study is also worth of looking.

Huang HY, Appel LJ. Supplementation of diets with alpha-tocopherol
reduces serum concentrations of gamma- and delta-tocopherol in humans. J
Nutr. 2003 Oct;133(10):3137-40.

Department of Epidemiology, Bloomberg School of Public Health, Johns
Hopkins University, Baltimore, MD 21205, USA.

Despite promising evidence from in vitro experiments and observational
studies, supplementation of diets with alpha-tocopherol has not reduced
the risk of cardiovascular disease and cancer in most large-scale
clinical trials. One plausible explanation is that the potential health
benefits of alpha-tocopherol supplements are offset by deleterious
changes in the bioavailability and/or bioactivity of other nutrients. We
studied the effects of supplementing diets with RRR-alpha-tocopheryl
acetate (400 IU/d) on serum concentrations of gamma- and
delta-tocopherol in a randomized, placebo-controlled trial in 184 adult
nonsmokers. Outcomes were changes in serum concentrations of gamma- and
delta-tocopherol from baseline to the end of the 2-mo experimental
period. Compared with placebo, supplementation with alpha-tocopherol
reduced serum gamma-tocopherol concentrations by a median change of 58%
[95% CI = (51%, 66%), P < 0.0001], and reduced the number of individuals
with detectable delta-tocopherol concentrations (P < 0.0001). Consistent
with trial results were the results from baseline cross-sectional
analyses, in which prior vitamin E supplement users had significantly
lower serum gamma-tocopherol than nonusers. In view of the potential
benefits of gamma- and delta-tocopherol, the efficacy of
alpha-tocopherol supplementation may be reduced due to decreases in
serum gamma- and delta-tocopherol levels. Additional research is clearly
warranted. PMID: 14519797

http://www.ncbi.nlm.nih.gov/entrez/q..._uids=14519797

--
Juhana

Please, enlighten me. Not all vitamin E supplements are created equal,
or the vitamin E in supplement form is not equivalent to that found in
natural food sources? Are you saying, one or the other or both? Maybe
neither?

Sbharris[atsign]ix.netcom.com wrote:
:: Look, if this study had been done with dl-alpha, critics would be
:: complaining it wasn't done with the ddd natural isomer. And since it
:: was done with the d,d,d, now they're complaining it wasn't done with
:: the proper "natural mix" of alpha, beta, gamma, and delta isomers
:: (whatever *that* is-- since it varies widely within different foods
:: and cultural food mixes, and the body can, and does, methylate the
:: more common natural gamma to more-needed and protein carrier specific
:: alpha). [...]

AFAIK, many, perhaps most health benefits of dietary vitamin E are
associated with gamma-tocopherol. Why do they keep doing studies with
supplemental alpha-tocopherol and even worse, dl-alpha? It makes me
suspect that they want to get negative results.

--
Juhana

montygram <nazztrader[at]lycos.com> wrote:
- quote -

Quite the opposite.

- quote -

Look, if this study had been done with dl-alpha, critics would be
complaining it wasn't done with the ddd natural isomer. And since it
was done with the d,d,d, now they're complaining it wasn't done with
the proper "natural mix" of alpha, beta, gamma, and delta isomers
(whatever *that* is-- since it varies widely within different foods and
cultural food mixes, and the body can, and does, methylate the more
common natural gamma to more-needed and protein carrier specific
alpha).

And if the study *had* been done with a 4 isomer mix, the critics would
be complaining that the negative result and the health problems were
due to the fact that it wasn't done with the 4 isomer mix with
chocolate sauce and a blueberry on top. It never ends. If *that* had
been the protocol, the critics would pooh pooh it for omitting a
sprinkling of sesame seeds, rice tocotrienols, and a partridge in a
pear tree.

Look, you health-gurus. Call your shots BEFOREHAND. Don't spend decades
playing up people like the Shutes, and then when they are proven
totally wrong, claim you never heard of them, and certainly didn't
support their views. Sheesh.

SBH

It's like these guys never read the scientific literature. I cited a
yet to be published study discussed on Dr. Mercola's site in my 2002
book. And similar claims like that have been made in the past.
Basicially, just like the phrase "saturated fat," there is no such
thing as "vitamin E." Instead, there are at least 4 major molecules
that are classified as "vitamin E," and if you get too much of one, it
can interfere with the actions of the others. Mostly, "vitamin E"
supplementation is done with the alpha form, which can deplete the
gamma form, and that can account for more deaths of particular causes.
Just avoid substances that cause oxidative stress, like unsaturated
fatty acids and oxidized cholesterol, and eat antioxidant rich foods
like blueberries and dark chocolate, and you'll do your body a big
favor.

Here's the abstract of the study, which is called HOPE-TOO (HOPE-The
Ongoing Outcomes = HOPE-TOO . It's an ongoing bit of the HOPE trial
(Heart Outcomes Prevention Evaluation). This is the biggest, longest
prospective blinded and placebo-controlled prospective trial of d-alpha
tocopherol acetate. Basically, vitamin E per se as the d-alpha
tocopherol has been found to do nothing particularly good in heart
disease or diabetes. Worse than that, it increases chance of congestive
heart failure (albeit of a probably mild type). My comments are
appended.


"Effects of Long-term Vitamin E Supplementation on Cardiovascular
Events and Cancer: A Randomized Controlled Trial" The HOPE and HOPE-TOO
Trial Investigators* JAMA, Vol. 293, pp. 1338-47 (March 15, 2005).

ABSTRACT:

Context: Experimental and epidemiological data suggest that Vitamin E
supplementation
may prevent cancer and cardiovascular events. Clinical trials have
generally failed to confirm benefits, possibly due to their relatively
short duration.

Objective: To evaluate whether long-term supplementation with Vitamin E
decreases the
risk of cancer, cancer death, and major cardiovascular events.

Design, Setting, and Patients: A randomized, double-blind,
placebo-controlled international trial (the initial Heart Outcomes
Prevention Evaluation [HOPE] trial conducted between December 21, 1993
and April 15, 1999) of patients at least 55 years old with vascular
disease or diabetes mellitus was extended (HOPE-The Ongoing Outcomes
[HOPE-TOO]) between April 16, 1999 and May 26, 2003.

Of the initial 267 HOPE centers that had enrolled 9,541 patients, 174
centers participated in the HOPE-TOO trial. Of 7,030 patients enrolled
at these centers, 916 were deceased at the beginning of the extension,
1,382 refused participation, 3,994 continued to take the study
intervention, and 738 agreed to passive follow-up. Median duration of
follow-up was 7.0 years.

Intervention: Daily dose of natural source Vitamin E (400 IU) [d-alpha
tocopherol acetate] or matching placebo.

Main Outcome Measures: Primary outcomes included cancer incidence,
cancer deaths, and major cardiovascular events (myocardial infarction,
stroke, and cardiovascular death). Secondary outcomes included heart
failure, unstable angina, and revascularizations.

Results: Among all HOPE patients, there were no significant
differences in the primary analysis: for cancer incidence, there were
552 patients (11.6%) in the Vitamin E group vs 586 (12.3%) in the
placebo group (relative risk [RR], 0.94; 95% confidence interval [CI],
0.84-1.06; P = .30); for cancer deaths, 156 (3.3%) vs 178 (3.7%),
respectively (RR, 0.88; 95% CI, 0.71-1.09; P = .24); and for major
cardiovascular events, 1022 (21.5%) vs 985 (20.6%), respectively (RR,
1.04; 95% CI, 0.96-1.14; P = .34). Patients in the Vitamin E group had
a higher risk of heart failure (RR, 1.13; 95% CI, 1.01-1.26; P = .03)
and hospitalization for heart failure (RR, 1.21; 95% CI, 1.00-1.47; P =
..045). Similarly, among patients enrolled at the centers participating
in the HOPE-TOO trial, there were no differences in cancer incidence,
cancer deaths, and major cardiovascular events, but higher rates of
heart failure and hospitalizations for heart failure.

Conclusion: In patients with vascular disease or Diabetes Mellitus,
long-term Vitamin E supplementation does not prevent cancer nor major
cardiovascular events and may increase the risk for heart failure.


==============================


COMMENT by S. Harris:

In the initial shorter duration version of the HOPE trial 3 years ago
(> 1800 patients per group), congestive heart failure (CHF) came closest
of any endpoint to being greater in the d-alpha tocopherol acetate 400
IU group, with the RR 1.21 and confidence limits 1.0 - 1.46) p = 0.05.
Hospitalization for CHF didn't come close to significance at p = 0.51.
With larger numbers and longer followup, both these are now significant
in the HOPE-TOO.

The interesting thing is that CHF is usually a consequence of coronary
disease and old MIs. But the number of MIs and other coronary events
really didn't come close to being significantly altered by the vitamin
E in the full study above (which is the only one I have access to,
right now). The closest of anything was stroke, which had a p of 0.2.
None of the cardiac stuff was much different from RR =1, so it does NOT
look like it was there, but just isn't showing above the noise due to
power problems.

So what's going on? Of course I have no idea. But this kind of
"congestive heart failure" is not as bad as it sounds to the layman, if
if doesn't increase deaths and doesn't result from any detectable
increase in coronary events. It basically means retention of fluid in
feet or lungs, and hospitalization means there's enough retention in
the lungs to cause problems. We have no way to know if in this study,
the extra cases were due to some global weakening of cardiac function,
or just some odd changes in salt handling and retention (which would of
course be less worrisome). We do know from this and many other studies
that blood pressure and renal function (at least, of the gross
filtration sort) are not affected at all by doses of vitamin E in this
range. So it's a mystery. Still, I'm not going to pretend even this
non-MI-related CHF is okay, although in many practices it would simply
mean an adjustment of diuretic. The bottom line is the only thing
vitamin E does for cardiac patients we can really be sure of, is
something (somewhat) bad.

The main value of these studies is to show that vitamin E as the
d-alpha form, in doses large enough to raise blood levels by 70%, has
NO effect on heart disease progression. Or on diabetes progression. Not
even a hint of it, in a placebo controlled study of many thousands of
people extending many years. I have a whole book (by Wilfred Shute,
M.D. with Harald Taub: _Vitamin E for Ailing and Healthy Hearts_ 1969,
with the 11th paperback printing I have from 1977) claiming that this
very d-alpha tocopherol in similar amounts, is a veritable cure-all for
all cardiac ailments. These claims by the Shute brothers go all the way
back to the 1940's. Every chapter of every health book since the Shutes
started blowing this horn, has had an enormous amount of junk
repetition of all these claims.

Well, these Shute claims appear to be wishful thinking. The real shame
is that it's taken the "medical establishment" half a century to prove
it. And no, there's still no good prospective evidence that vitamin E
prevents cancer in humans, either. (Frankly, I'm a little more hopeful
that selenium will prove out, there. And possibly even vitamin C.)
Vitamin E per se in reasonable and traditional supplemental amounts
(which 400 IU is) certainly doesn't affect onset of diabetes, or
progression of diabetic renal disease. We know that from the HOPE trial
also. I would have wagered a modest amount of money that this wouldn't
be so, from what I know of oxidative mechanisms in diabetes. But I'd
have been wrong. That's why we do these studies.

And no, the HOPE trial goes beyond showing that vitamin E just doesn't
heal the diseased-of-heart (though the Shutes claimed just that). Most
of the HOPE enrollees were not clinically ill, though they did have
coronary disease. If vitamin E even slowed progression of those with
disease, it would have been seen here. It wasn't. The idea that vitamin
E prevents ONSET of coronary disease in totally healthy people who
don't have any at all (if such adults exist in our society), *even
though* it doesn't at all effect progression of disease in people who
already have some, is very far fetched. I think it's grasping at
straws, in fact. I don't believe it, and can't imagine why anybody
would.

Here's the full text of the first phase of the HOPE trial, for the
vitamin E side (as you know, there was another side looking at
preventive effects of giving the ACE inhibitor ramepril).

http://care.diabetesjournals.org/cgi...ull/25/11/1919

SBH