EU vitamin ban -can cutting vitamin intake be dangerous?
Hugh Easton
passed a directive that will make any dietary supplement containing
more than the E.U. recommended daily vitamin allowance illegal. For
vitamin E, the RDA is (I think) 15 IU. My current vitamin E intake is
therefore almost 30 times higher than what will be allowable under the
new regulations. Is there any potential danger in reducing intake of
an important antioxidant vitamin by such a large amount? A google
search shows that "rebound deficiency" does occur with vitamin E, and
the possible effects sound unpleasant, to say the least:
Deficiency symptoms include: (rebound symptoms, if large doses are
halted abruptly), anemia, degenerating muscles, muscular weakness,
sore muscles, charley horse, ceroid deposits in muscles, degenerating
endocrine glands, sterility, degenerating peripheral vascular system,
deterioration of nervous system, angina, decreased survival time of
red blood cells, RBC rupture, increased creatinine in urine, acne,
increased need for oxygen, slow healing, scars/stretch marks remain,
wrinkled skin, decreased ozone/radiation/cancer resistance.
I have been taking between 400 and 500 iu of vitamin E daily for more
than 15 years now, and it seems to me that going from that to the EU
RDA carries a high risk of rebound effects. I get the impression that
rebound deficiency isn't a very well studied phenomenon, and that I
(and everyone else affected by the EU ban) will be unwilling guinea
pigs in a huge unplanned experiment.
Given the fact that vitamin E has an excellent safety record in the
dosage range I am taking, my preference would be to just keep taking
the 400 iu daily on an indefinite basis rather than risk cancer,
sterility and degeneration of my nervous system. Does anyone know if
that will be possible after the new regulations come into effect, and
if so, how?
Steve Harris
"Hugh Easton" <might...@yahoo.co.uk> wrote in message
news:3c911b90...@news.eurobell.co.uk...
> I'm currently taking 400 iu of vitamin E daily. The EU have just
> passed a directive that will make any dietary supplement containing
> more than the E.U. recommended daily vitamin allowance illegal. For
> vitamin E, the RDA is (I think) 15 IU. My current vitamin E intake is
> therefore almost 30 times higher than what will be allowable under the
> new regulations. Is there any potential danger in reducing intake of
> an important antioxidant vitamin by such a large amount? A google
> search shows that "rebound deficiency" does occur with vitamin E, and
> the possible effects sound unpleasant, to say the least:
>
> Deficiency symptoms include: (rebound symptoms, if large doses are
> halted abruptly), anemia, degenerating muscles, muscular weakness,
> sore muscles, charley horse, ceroid deposits in muscles, degenerating
> endocrine glands, sterility, degenerating peripheral vascular system,
> deterioration of nervous system, angina, decreased survival time of
> red blood cells, RBC rupture, increased creatinine in urine, acne,
> increased need for oxygen, slow healing, scars/stretch marks remain,
> wrinkled skin, decreased ozone/radiation/cancer resistance.
Comment: This is why they call it the Net of a Million Lies. You're reading
this off the Innvista site, and they don't give a reference, and I
personally think they need to sit down and take a Stress Pill. You, too.
No, you don't like that. Okay, Hugh, I won't lie to you. You're in for a
horrible, absolutely gruesome malnutritional oxidative death. About 3 days
after the EU law takes away your vitamin E pills, you're going to wake up
and find your hair all white! It litters your pillow! You feel wrinkles
crawl across your bloodless face, like worms, and your private parts shrivel
into insignificance. As you rise to go to the bathroom, you see an old man
coming toward you. You spit out your loosening teeth and as you close on
this apparition, you notice you can't focus on the mirror. Lucky for you....
Don't forget to write us here, with your festering nubs of fingers smearing
the keys with loathsome fluids, and tell us all the details.
SBH
--
I welcome Email from strangers with the minimal cleverness to fix my address
(it's an open-book test). I strongly recommend recipients of unsolicited
bulk Email ad spam use "http://combat.uxn.com" to get the true corporate
name of the last ISP address on the viewsource header, then forward message
& headers to "abuse@[offendingISP]."
Kurt Ullman
<sbha...@ix.RETICULATEDOBJECTcom.com> wrote:
>No, you don't like that. Okay, Hugh, I won't lie to you. You're in for a
>horrible, absolutely gruesome malnutritional oxidative death. About 3 days
>after the EU law takes away your vitamin E pills, you're going to wake up
>and find your hair all white! It litters your pillow! You feel wrinkles
>crawl across your bloodless face, like worms, and your private parts shrivel
>into insignificance. As you rise to go to the bathroom, you see an old man
>coming toward you. You spit out your loosening teeth and as you close on
>this apparition, you notice you can't focus on the mirror. Lucky for you....
>
I take it that's a "no"???
----------------------------------
This mail is a natural product. The slight variations in spelling and
grammar enhance its individual character and beauty and in no way are to
be considered flaws or defects.
andrew fox
anyway?
andrew
Dave B
> what the hell are you doing taking 30 times the recommended daily dose
> anyway?
>
> andrew
He's certainly going against the grain. I don't like it any more than you.
But what can be done? People like that are on a death wish and nothing will
save them short of government intervention.
Dave B.
CharlesSWaters
--
Cheerio,
Charles
"Question with boldness even the very existence of a God; because if there
be one, he must more approve of the homage of reason than that of a
blindfolded fear." -- Thomas Jefferson
"andrew fox" <andrewi...@ntlworld.com> wrote in message
news:3C923C6...@ntlworld.com...
suzee
>
> RDA is minimum, not optimum.
>
> --
As I understand it, the RDA is what will keep you alive - not
necessarily in the best of health. It used to be called the *minimum*
daily allowance. The name was changed to *required* which makes one
think that's all that's needed.
sue
Steve Harris
news:3C9586...@nidlink.com...
No. The only kind of "RDA" that still exists, the Recommended *DAILY*
Allowance, is set at the top of the DRI (Dietary Reference Intake) range for
most (ie, nonpregnant o lactating) people. That RDailyA is still around so
that authorities can have a single number they can put on the side of a box,
with a % of that, per serving. This number is the one for the age group
which needs the most of that stuff (except for pregnant or lactating women)
and will be high for most all other groups (except as noted). Effectively,
the RDailyAs are usually set by the needs of men, except for calcium, which
is set a little higher, due to the needs of women.
It was the old RDA, the Recommended DIETARY Allowance, was less than our
modern version of the RDA, but still not a minimum.
The DRI takes into account age and reproductive status, and is a range, all
less than the RDailyA (except as noted). None of these numbers is a minimum,
but rather the number likely to result in good body loading for a given
nutrient, for nearly everyone described in the reference population.
The idea of RDAs (of either sort) as a minimum was always a big nutritional
myth, however. Nutritionists have always known better, but the public still
hasn't gotten the message.
Thomas Carter
> >
> > As I understand it, the RDA is what will keep you alive - not
> > necessarily in the best of health. It used to be called the *minimum*
> > daily allowance. The name was changed to *required* which makes one
> > think that's all that's needed.
> >
> > sue
>
> No. The only kind of "RDA" that still exists, the Recommended *DAILY*
> Allowance, is set at the top of the DRI (Dietary Reference Intake) range for
> most (ie, nonpregnant o lactating) people. That RDailyA is still around so
> that authorities can have a single number they can put on the side of a box,
> with a % of that, per serving. This number is the one for the age group
> which needs the most of that stuff (except for pregnant or lactating women)
> and will be high for most all other groups (except as noted). Effectively,
> the RDailyAs are usually set by the needs of men, except for calcium, which
> is set a little higher, due to the needs of women.
>
> It was the old RDA, the Recommended DIETARY Allowance, was less than our
> modern version of the RDA, but still not a minimum.
Hi Steve,
You and other anti vitamin zealots are the only ones in the country
who claim to not understand that the RDA or DRI or whatever its
current name might be is a minimum. They have now set maximums for
most of the common nutrients. The maximum for vit. C is now two grams.
>
> The DRI takes into account age and reproductive status, and is a range, all
> less than the RDailyA (except as noted). None of these numbers is a minimum,
> but rather the number likely to result in good body loading for a given
> nutrient, for nearly everyone described in the reference population.
>
There is no such thing as THE number likely to result in good body
loading and we all know it. If there was I would have to be careful
not to eat a large orange and a tomato on the same day or I would
ingest more C than THE number and not have good body loading.
> The idea of RDAs (of either sort) as a minimum was always a big nutritional
> myth, however. Nutritionists have always known better, but the public still
> hasn't gotten the message.
>
> SBH
The idea of RDAs as an optimum or anything else but a minimum is a
silly and obvious construct of the anti vitamin crowd. Nutritionists
have always known better. The public will never be fooled on this, but
the "hate vitamins till I die crowd" will never get the message.
You have a lot to add to this group, but your message will sell better
if you come down off the podium and keep your feet on the ground.
Thomas
Steve Harris
>"Steve Harris" <sbha...@ix.RETICULATEDOBJECTcom.com> wrote in message
news:<a75l78$d56$1...@nntp9.atl.mindspring.net>...
>> Allowance, is set at the top of the DRI (Dietary Reference Intake) range
for
>> most (ie, nonpregnant o lactating) people. That RDailyA is still around
so
>> that authorities can have a single number they can put on the side of a
box,
>> with a % of that, per serving. This number is the one for the age group
>> which needs the most of that stuff (except for pregnant or lactating
women)
>> and will be high for most all other groups (except as noted).
Effectively,
>> the RDailyAs are usually set by the needs of men, except for calcium,
which
>> is set a little higher, due to the needs of women.
>>
>> It was the old RDA, the Recommended DIETARY Allowance, was less than our
>> modern version of the RDA, but still not a minimum.
>
>Hi Steve,
>You and other anti vitamin zealots are the only ones in the country
>who claim to not understand that the RDA or DRI or whatever its
>current name might be is a minimum. They have now set maximums for
>most of the common nutrients. The maximum for vit. C is now two grams.
So what? Because the DRI is not the maximum, you think it must be a
minimum? Are you satisfied with the logic of that?
>> The DRI takes into account age and reproductive status, and is a range,
all
>> less than the RDailyA (except as noted). None of these numbers is a
minimum,
>> but rather the number likely to result in good body loading for a given
>> nutrient, for nearly everyone described in the reference population.
>>
>There is no such thing as THE number likely to result in good body
>loading and we all know it.
Maybe you don't. But then again, you may be uneducable.
>If there was I would have to be careful
>not to eat a large orange and a tomato on the same day or I would
>ingest more C than THE number and not have good body loading.
You've have much the same body load (stores) of vitamin C if you ate 6
oranges a day as if you ate one. That's the point. It's an S-shaped
(sigmoidal) curve and you get 80 or 90% of the body stores from 100 mg of
vitamin C a day as if you eat 2 grams. The DRI/RDA is merely the number that
results in tanking most people nearly all the way up (which would happen
above 250 mg/day). Without (I might add) putting them into the range where
they start metabolizing it faster so they are at risk of rebound
hypovitaminosis if they do go back to eating a normal nonsupplented diet.
If you want to become megadose-dependent, be my guest. But I think it's
rather unnatural.
I'm on record as suggesting that it might be better to take supplements in
doses sufficient to just saturate your body stores, perhaps a few times a
week. By doing that, I think you might be able get the best of both worlds.
>The idea of RDAs as an optimum or anything else but a minimum is a
>silly and obvious construct of the anti vitamin crowd. Nutritionists
>have always known better.
Bologna.
--
I welcome email from any being clever enough to fix my address. It's open
book. A prize to the first spambot that passes my Turing test.
michaelprice
> You've have much the same body load (stores) of vitamin C if you ate 6
> oranges a day as if you ate one. That's the point. It's an S-shaped
> (sigmoidal) curve and you get 80 or 90% of the body stores from 100 mg of
> vitamin C a day as if you eat 2 grams.
Have you a reference for that?
Cheers,
Michael C Price
Scottie
What a crock of shit Steve!
What is your purpose here in the sci.life extension newsgroup other than to
slash the legs off a snowballing industry. Some of your references are
clearly non-factual. Who cares if you have 200 references all backing up
your point - it can't change the fact that RDI's are way outdated - they
were set before the vietnam war and have changed little since.
If taking high doses of Vitamin E has kept this guy going for 15 years
after all that WAS the purpose of this whole discussion) and he has found
benefits then what is your point?
Your cinical repsonse to his first posting typifies the response of the
mis-informed.
http://www.drlam.com/supplements/oda.cfm
Websites don't exist like this just for fun!
Trevor
Steve Harris
>
>What a crock of shit Steve!
>Your cinical repsonse to his first posting typifies the response of the
>mis-informed.
>http://www.drlam.com/supplements/oda.cfm
>Websites don't exist like this just for fun!
No, they exist to make money. It's DrLam.com not DrLam.charity. This site
advertises Dr. Lam, who is supposedly a "board certified anti-aging doctor."
Alas, there are no such boards given by any standard medical society or by
the American Board of Internal Medicine. There are some quack boards, of
course. And there's the A4M which is a hotbed of quacks. Last time I was
there, there were darkfield microscopes and electric gizmos galore. All to
make you younger and cure your hidden diseases. ROFL.
SBH
Scottie
Fair enough! I respect your view after citing some of your references. You
have your point of view and I have mine. I'm not quite sure that yours is to
the success of this newsgroup as one would hope! I disagree with megadosing,
but I do agree with taking far higher rates than those people who post RDI's
would have us believe. That's why I do this...
http://www.reliv.com/inside/productstable.html
Have been for 5 years and have gone to the doc every year since and he can't
believe me going from 5 different medications to none in 3 weeks. I was
spiraling downhill quickly and nothing helped. I saw incredible results in
under 48 hours. That got my attention!
Trevor
Dave B
> No, they exist to make money. It's DrLam.com not DrLam.charity. This site
> advertises Dr. Lam, who is supposedly a "board certified anti-aging
> doctor." Alas, there are no such boards given by any standard medical
> society or by
> the American Board of Internal Medicine. There are some quack boards, of
> course. And there's the A4M which is a hotbed of quacks. Last time I was
> there, there were darkfield microscopes and electric gizmos galore. All
> to
> make you younger and cure your hidden diseases. ROFL.
Another technique used by some of these 'quacks' is to actually treat their
patients with respect and dignity. To talk with them on the same level and
ease their mind. And to give them a sense of hope.
John 'the Man'
Once upon a time, our fellow Scottie
rambled on about "Re: EU vitamin ban -can cutting vitamin intake be
dangerous?."
Our champion being bored in sci.med.nutrition retorts, thusly ...
>What a crock of shit Steve!
I will second that opinion! :-)
--
John Gohde,
Achieving good Nutrition is an Art, NOT a Science!
My hidden agenda is to improve my personal health. Beware of anybody
who brags about eating a lousy diet or smoking.
www.Food.NaturalHealthPerspective.com/
Presenting great rules of thumb to eat by!
michaelprice
> No, they exist to make money. It's DrLam.com not DrLam.charity. This site
> advertises Dr. Lam,
Having a website is a sin?
> who is supposedly a "board certified anti-aging doctor."
> Alas, there are no such boards given by any standard medical society or by
> the American Board of Internal Medicine.
Any of the above endorse cryonics, Steve?
Does that mean cryonics is bunk?
Here's is Dr Lam's profile (from his website):
Michael Lam, M.D., M.P.H., A.B.A.A.M. is a specialist in Preventive and
Anti-Aging Medicine. He is currently the Director of Medical Education at
the Academy of Anti-Aging Research, U.S.A. He received his Bachelor of
Science degree from Oregon State University, and his Doctor of Medicine
degree from Loma Linda University School of Medicine, California. He also
holds a Masters of Public Health degree and is Board Certification in
Anti-aging Medicine by the American Board of Anti-Aging Medicine. Dr. Lam
pioneered the formulation of the three clinical phases of aging as well as
the concept of diagnosis and treatment of sub-clinical age related
degenerative diseases to deter the aging process. Dr. Lam has been published
extensively in this field. He is the author of The Five Proven Secrets to
Longevity (available on-line). He also serves as editor of the Journal of
Anti-Aging Research
Cheers,
Michael C Price
Max Watt
> RDA is minimum, not optimum.
>
> --
Dr. Steve Harris explained that RDA is above minimum for most, but not
all people. Which is not to say that it is optimum.
About two years ago someone posted here (sci.life-extension) a
longevity versus vitamin usage meta-study; the only anti0xidant whose
use consistently increased longevity was vitamin E, and much more
weakly, vitamin C, but only when combined with E. We also had a
recent post of a study where E intake was optimized at 200 IU a day;
larger doses were counter productive. (Most E supplements come at 400
units, next most popular size is 100 units.)
Optimum is going to be hard to determine, and what's good for the
general population may not be right for an individual. The husband of
a coworker of mine developed tachycardia and spend some time in
hospital before it was determined that his vitamin E supplement was
causing the problem. It's not good for everyone.
I believe there is now a Journal of Optimum Nutrition, but I don't
know how much about it.
As for the EU banning pills larger than the RDA, one could just make
very tiny pills, and those who want more can measure them out with a
measuring spoon and swallow a dozen at once.
Steve Harris
<39Xl8.8097$WP.17...@news2-win.server.ntlworld.com>...
>"Steve Harris" <sbha...@ix.RETICULATEDOBJECTcom.com> wrote in message
>news:a78rr1$4m0
>
>> No, they exist to make money. It's DrLam.com not DrLam.charity. This
site
>> advertises Dr. Lam,
>
>Having a website is a sin?
Never said it was. This is an advertisement center for a business.
>> who is supposedly a "board certified anti-aging doctor."
>> Alas, there are no such boards given by any standard medical society or
by
>> the American Board of Internal Medicine.
>Any of the above endorse cryonics, Steve?
>Does that mean cryonics is bunk?
No, but it does mean cryonics is an experiment with no good evidence behind
it. It has to be, since the end of the experiment involves technology that
hasn't been invented yet. Meanwhile, there are no promises in cryonics
except to try to get you into the future without thawing out.
Experiments in which you pay money to get in to the trial, should be sold as
experiments. Cryonics generally is. How could it not be? And experiments
are more or less appropriate and ethical depending on the problem being
treated. People who are clinically dead have a big medical problem, and the
downside to going nothing is that you merely stay dead. This puts it in a
quite different category from trying things while you're alive that could be
dangerous. The only thing I've never heard as a criticism of cryonics is
that it's dangerous. I wish I could say the same about growth hormone and
testosterone.
>Here's is Dr Lam's profile (from his website):
>Michael Lam, M.D., M.P.H., A.B.A.A.M. is a specialist in Preventive and
>Anti-Aging Medicine.
How can you be a specialist in anti-aging medicine, when no treatment has
been shown to slow aging in humans? In animals, there's dietary
restriction-- but I doubt this guy runs a weight loss clinic.
>He is currently the Director of Medical Education at
>the Academy of Anti-Aging Research, U.S.A.
That's nice. So? I'm director of the American Academy of Superheros
(League of Justice Division). Wanna see our letterhead? Wanna see my cape?
> He received his Bachelor of
>Science degree from Oregon State University, and his Doctor of Medicine
>degree from Loma Linda University School of Medicine, California.
Well, then, he's well prepared to preach prevension and the SDA Jesus.
> He also
>holds a Masters of Public Health degree
From where?
> and is Board Certification in
>Anti-aging Medicine by the American Board of Anti-Aging Medicine.
Ye Quack organization. Since nobody knows how to interfere with aging in
humans, such a certification is the one I have for the Academy of Leaping
Tall Buildings in a Single Bound. Just don't as me for a demo.
> Dr. Lam
>pioneered the formulation of the three clinical phases of aging as well as
>the concept of diagnosis and treatment of sub-clinical age related
>degenerative diseases to deter the aging process.
Published in the New England Journal. Not.
> Dr. Lam has been published
>extensively in this field.
In quack journals.
He is the author of The Five Proven Secrets to
>Longevity (available on-line).
No doubt. Sure as hell is no something your're going to find in your local
medical bookstore.
>He also serves as editor of the Journal of
>Anti-Aging Research
Well, that should help him get his articles published there, then. Did you
know there's a Journal of Homeopathy, too?
Chuck
LEF had an article several months ago that mentioned a study that
measured the immune systems of elderly people and it took 800 iu to
get the benefits of an enhanced immune system. I wouldn't think that
800 iu would be counterproductive but then again I hear a lot of
different opinions lately.
Dave B
> dangerous. The only thing I've never heard as a criticism of cryonics is
> that it's dangerous. I wish I could say the same about growth hormone and
> testosterone.
Again with the hormones? Bad high school gym memories? Who is dying of
steroids or growth hormone? Bodybuilders use higher doses than you would
dare give to your frozen dogs. Yet they seem to be doing pretty well. Sure
they will probably die sooner. But what retirement home would have room for
those freaks anyway?
You must have quite a time deciding whether you should leave your home and
risk getting hit by a meteorite or staying put and running the risk of
radon inhalation.
>>He is currently the Director of Medical Education at
>>the Academy of Anti-Aging Research, U.S.A.
>
> That's nice. So? I'm director of the American Academy of Superheros
> (League of Justice Division). Wanna see our letterhead? Wanna see my
> cape?
LOL!
Max Watt
> maxwa...@yahoo.com (Max Watt) wrote in message news:<870a5d01.02032...@posting.google.com>...
> > "CharlesSWaters" <cswater...@newsguy.com> wrote in message news:<a73s6...@enews2.newsguy.com>...
> LEF had an article several months ago that mentioned a study that
> measured the immune systems of elderly people and it took 800 iu to
> get the benefits of an enhanced immune system. I wouldn't think that
> 800 iu would be counterproductive but then again I hear a lot of
> different opinions lately.
One size does not fit all.
Max Watt
> Snobs be gone!
>
> Once upon a time, our fellow Scottie
Och, Aye thought ye were an Indian Hindu vegetarian!
Dave B
> About two years ago someone posted here (sci.life-extension) a
> longevity versus vitamin usage meta-study; the only anti0xidant whose
> use consistently increased longevity was vitamin E, and much more
> weakly, vitamin C, but only when combined with E. We also had a
> recent post of a study where E intake was optimized at 200 IU a day;
> larger doses were counter productive. (Most E supplements come at 400
> units, next most popular size is 100 units.)
Keep in mind that these Vitamin E supplements are incomplete. There are at
least 8 forms. High doses of the alpha alone might be displacing other
tocopherols.
michaelprice
> You've have much the same body load (stores) of vitamin C if you ate 6
> oranges a day as if you ate one. That's the point. It's an S-shaped
> (sigmoidal) curve and you get 80 or 90% of the body stores from 100 mg of
> vitamin C a day as if you eat 2 grams.
Me:
> Have you a reference for that?
And a further thought. Over what time-scales where the experiments which
Steve bases his conclusions on? It takes the human body years to fully
respond to increased vitamin C intake. I quote
"Vitamin C supplementation [500 mg.day] elevated plasma total ascorbate
level
by 30.1% (P:=0.043) in 12 months and
by 91.1% (P:=0. 001) in 36 months"
See:
Long-term effects of vitamin E, vitamin C, and combined supplementation on
urinary 7-hydro-8-oxo-2'-deoxyguanosine, serum cholesterol oxidation
products, and oxidation resistance of lipids in nondepleted men.
Porkkala-Sarataho E, Salonen JT, Nyyssonen K, Kaikkonen J, Salonen R,
Ristonmaa U, Diczfalusy U, Brigelius-Flohe R, Loft S, Poulsen HE.
Research Institute of Public Health, University of Kuopio, Kuopio, Finland.
We studied the long-term effects of vitamins E and C and their combination
on lipid peroxidation in vivo and in vitro. The Antioxidant Supplementation
in Atherosclerosis Prevention (ASAP) trial is a double-masked
placebo-controlled randomized clinical trial to study the effects of vitamin
C (500 mg of slow release ascorbate per day), vitamin E (182 mg of
RRR-alpha-tocopherol acetate per day), and the combination of both
antioxidants. Lipid peroxidation measurements were carried out for 48 male
participants at entry and at 12 and 36 months. Compared with placebo,
vitamin E and the vitamin combination increased plasma lipid-standardized
alpha-tocopherol during the first 12 months by 68.2% and 65.2% (P:<0. 001
for both), respectively, and reduced serum 7beta-hydroxycholesterol by 50.4%
(P:=0.013) and 44.0% (P:=0.041), respectively. The net change of lipid
standardized alpha-tocopherol was 63.8% after 36 months of vitamin E
supplementation and 43.3% for the combination. Vitamin C supplementation
elevated plasma total ascorbate level by 30.1% (P:=0.043) in 12 months and
by 91.1% (P:=0. 001) in 36 months. Neither vitamin E, vitamin C, nor the
combination influenced the urinary excretion rate of
7-hydro-8-oxo-2'-deoxyguanosine or the antioxidative capacity of plasma.
Vitamin E and the combination of vitamins E and C enhanced the oxidation
resistance of isolated lipoproteins and total serum lipids. Our data
indicate that long-term supplementation of nondepleted men with a reasonable
dose of vitamin E alone or in combination with slow release vitamin C
reduces lipid peroxidation in vitro and in vivo, whereas a relatively high
dose of vitamin C alone does not.
Publication Types:
Clinical Trial
Randomized Controlled Trial
PMID: 10978253 [PubMed - indexed for MEDLINE]
Cheers,
Michael C Price
Martin Banschbach
Dave, you make a very good point. I thought that the ethical vegans
were wacked out. These life extension people are even more wacho.
I know that I'm going to get a good ass wooping. We have a guy on
a local radio station that calls people up cold (companies) and
tells them that they have done something wrong and are going to
get a real ass wooping. This guy and this station are tops in
the local market. Of course all of his calls are broadcast live
and I must admitt that I get a real kick out of how people
respond to him. I don't know how much money he is paid to do
this but based on the fact that he is on in multiple markets,
it's probably a pretty penny.
Vegans, even if they do it for ethical reasons, are on a very good
diet (for adults). You poor fools are popping pills left and right
with no idea how much harm you are really doing to your body.
In my old age, I am starting to identify with people that
care about animals. Life extension folks are really sick in
my opinion. There has to be more than 1 screw loose to
adopt this kind of mentality.
Max Watt
Maybe that's why vitamin E doses of > 200 mg daily appear to be
counterproductive. It is known that large doses of alpha-tocopherol
drives out gamma-tocopherol from certain tissues, and gamma-tocopherol
does have some benefical effects alpha- does not. Not to mention the
tocotrienols, present in "natural E complex", or in food.
On the other hand, there are definite benefits with a certain level of
E supplementation, for cardiovascular health, and it is impossible to
to get what appears to be the optimum level of about 200 mg from food
alone.
Dave B
As one of those fools, I'm having some mixed feelings about your post. I
just meant they should take high doses of the other forms as well. :-)
Steve Harris
<870a5d01.02032...@posting.google.com>...
>Maybe that's why vitamin E doses of > 200 mg daily appear to be
>counterproductive
More likely it's exactly what we've been talking about. Vitamin E has a U
shaped effect on the immune system. Some improves your immune function.
Take too much and you sop up enough radicals to actually begin to degrade
response again (ie, it's anti-inflammatory and immune suppressive). Again,
inflammation and a better immune response are closely related-- you don't
get to willy-nilly turn up one without effecting the other. There's no free
lunch, and high dose vitamin E is no exception.
Dave B
Evidence? Oh yeah, your own unpublished zombie dog popsicle experiments.
Tom Matthews
> Max Watt wrote in message
> <870a5d01.02032...@posting.google.com>...
>
>
>>Maybe that's why vitamin E doses of > 200 mg daily appear to be
>>counterproductive
>>
>
>
> More likely it's exactly what we've been talking about. Vitamin E has a U
> shaped effect on the immune system. Some improves your immune function.
> Take too much and you sop up enough radicals to actually begin to degrade
> response again (ie, it's anti-inflammatory and immune suppressive). Again,
> inflammation and a better immune response are closely related-- you don't
> get to willy-nilly turn up one without effecting the other. There's no free
> lunch, and high dose vitamin E is no exception.
I have no idea why you continue to insist that such scenarios are "more
likely". Not only do the various E vitamers have seriously different
effects, but there is excellent evidence to support their
interdependence (not to mention their relationships with other vitamins
and nutrients).
Of course, "there is no free lunch"! One cannot willy-nilly simply take
large doses of any one particular vitamin or nutrient without some
downsides! *Everything* has a U shaped dose/effect curve. To use a
phrase that I learned from you: "the dose makes the poison". However,
this does not preclude the possibility of beneficially taking a selected
combination of vitamins and nutrients at above food obtainable levels,
by intelligently reading the research and using it to guide one's
choices. To think that such is not possible (as you appear to do) is to
embrace an extremely negative, pessimistic and cynical world-view (which
you again appear to do - perhaps because of your own advancing age and
declining physical condition - I hardly recognized your new picture.
BTW, a little CR would help you a lot.).
*That* is what we are arguing may well be possible today and, in fact,
has some reasonable amount of evidence in its favor. And neither you nor
anyone else can express more than an *opinion* that we are wrong.
--Tom Matthews
MoreLife for us all - http://morelife.org
Reality based tools for More Life in quantity & quality
Max Watt
> Max Watt wrote in message
> <870a5d01.02032...@posting.google.com>...
>
> >Maybe that's why vitamin E doses of > 200 mg daily appear to be
> >counterproductive
>
>
> More likely it's exactly what we've been talking about.
That's the mechanism, in this case, that explains what you've been
talking about.
>Vitamin E has a U
> shaped effect on the immune system. Some improves your immune function.
> Take too much and you sop up enough radicals to actually begin to degrade
> response again (ie, it's anti-inflammatory and immune suppressive). Again,
> inflammation and a better immune response are closely related-- you don't
> get to willy-nilly turn up one without effecting the other. There's no free
> lunch, and high dose vitamin E is no exception.
Moderation in all things. But won't one man's high dose be another's
optimum level? Some people benefit more from high folate levels than
others due to a genetic lack of some enzyme or other (that was in one
of last month's theads.) Not only is the lunch not free, but the cost
seems to vary with the customer.
Steve Harris
>I have no idea why you continue to insist that such scenarios are "more
>likely". Not only do the various E vitamers have seriously different
>effects, but there is excellent evidence to support their
>interdependence (not to mention their relationships with other vitamins
>and nutrients).
COMMENT:
I think "interdependence" is a strong word and probably a bad and misleading
word for lack of total pharmacokinetic and pharmacodynamic independence.
Very few things have total pharmacologic independence, and good examples are
interactions between metabolism of numerous man-made drugs and various
nutrients. Levels of some go up, others down when the vitamin is given in
large amounts. None of which mean in the least that evolution has designed
in some "interdependence" of these things-- obviously for man-made drugs
this is not the case. But similar such findings are used to support supposed
interdependence of E vitamers. That's bad reasoning.
There is an alpha tocopherol binding protein which picks this vitamer up
preferentially, suggesting that this is the one the body prefers. There is
NO evidence that the body needs any other vitamer. There are no deficiency
symptoms or signs or any other problems known in animals not getting the
other vitamers. Life span studies done by myself and many other researchers
show perfectly normal life span studies with alpha tocopherol primarly (and
for that matter, these studies have classically been done with the dl,dl,dl
8-isomer mix, only one of which is found in nature). Possibly the animals
also get some gamma from the corn oil typically used in them as fat source,
but it's not much. The life span controls for these studies are those
historical studies in the pre-chow era, in which animals got mixed food
diets, where the E is mostly gamma-E. Life span's weren't any better, and
were usually worse.
We know from the reproductive studies that any active E vitomer is able to
substitute for any other, to the limit of delectability of pathology. One
study has been done in which animals were raised for 3 generations on
nothing but gamma-E. They did fine, but apparently were able to convert
some gamma to alpha-E. Again this suggests that alpha-E is what the body
prefers (for storage if for nothing else). That's it. Claims for a
specific nutritional need for gamma-E or tocotrienols rest on test tube
science or shaky post-hoc epidemiology, all of which are always insecure, to
say the least. Frankly I don't believe them, due to the gold-standard
semi-synthetic diet life span study results.
>Of course, "there is no free lunch"! One cannot willy-nilly simply take
>large doses of any one particular vitamin or nutrient without some
>downsides! *Everything* has a U shaped dose/effect curve. To use a
>phrase that I learned from you: "the dose makes the poison". However,
>this does not preclude the possibility of beneficially taking a selected
>combination of vitamins and nutrients at above food obtainable levels,
>by intelligently reading the research and using it to guide one's
>choices. To think that such is not possible (as you appear to do) is to
>embrace an extremely negative, pessimistic and cynical world-view (which
>you again appear to do - perhaps because of your own advancing age and
>declining physical condition - I hardly recognized your new picture.
>BTW, a little CR would help you a lot.).
No, now, ad hominem. Yes, nearing age 45 I've certainly lost my boyish
charm (unlike you, "Tom," who at age 45 were no doubt still being mistaken
for 25. Not). Today's newsflash: that tends to happen to us humans (take a
look at Bill Gates, Michael J. Fox, Pearson and Shaw, and basically most
people of average genetics who haven't had plastic surgery). No, I don't
like it. And yes, in fact, I am on a diet. And no, I refuse to dye my hair
or have a facelift. Graying hair is not fixable with nutrition; the
middle-age spread of course is. But it's also mostly cosmetic and low
levels. My physical condition is fine. I know because I'm not dead, having
recently subjected my body to learning scuba. This is not tropical
paddling, but diving in the West coast Pacific, to depths below 100 ft, in
water at depth around 60 F (15 C). Lots of fun, but (by the way) a place
where you're glad for every pound of extra fat-- it's not going to be nearly
as much fun when I'm skinnier. Caloric restriction (CR) may be great if you
want to sit in a nice climate-controlled lab basement or a sealed controlled
experiment in some warm place like Biosphere II. However, In other places--
on top of a mountain in the snow, under a lot of cold water in the Pacific,
or with a nasty infection-- you may well pay a price for CR that you hadn't
counted on. That is why I'm particularly watching you restricted Canucks--
the first one of you that crumps from infection is going to be editorialized
by moi. If I die first of a heart attack you can do the same for me, but
don't hold your breath-- my numbers are perfect.
>*That* is what we are arguing may well be possible today and, in fact,
>has some reasonable amount of evidence in its favor. And neither you nor
>anyone else can express more than an *opinion* that we are wrong.
That it's my "opinion" goes without saying. But burden of evidence is on
you, not me. I've given you my reasoning. The gold standard in experimental
gerontology- failing actual human trial results-- is mammalian life span
studies using long-lived strains. Vitamin-wise, they don't argue for your
side, but mine. So far as CR goes, rodent studies argue for your view in
controlled conditions, and primate studies are on-going (too early to tell;
biomarkers look good, but they too are being pampered). I think the jury's
still out for the real world and humans. You may well be right. Or you may
well be wrong. Again, I have little doubt that we're in for a lot of CR
people dying of funny diseases, while all the while their compadres are
saying "Well, if it wasn't for THAT freak thing, he'd have gotten to 150!"
But that's not the way it works. In the real world, there's a U-shaped
survival curve for body mass index, too, and it's not where CR would
predict. CR's advocates have a lot of explanation for that (ho hum-- maybe
enough vitamins weren't being taken; that's what life-extenders ALWAYS say),
but butt they remain ad-hoc apologias for now. I believe some of them, and
others not. I retain skepticism also. I've seen a lot of great theories in
medicine go down the tubes, and others succeed. Which was going to succeed
was by no means obvious, until the final results were in.
SBH
michaelprice
> That it's my "opinion" goes without saying. But burden of evidence
> is on you, not me. I've given you my reasoning. The gold standard
> in experimental gerontology- failing actual human trial results-- is
> mammalian life span studies using long-lived strains. Vitamin-wise,
> they don't argue for your side, but mine.
Steve, can you please explain the deficiencies of these three experiments:
Effect of pantothenic acid on the longevity of mice by Richard B Pelton and
Roger J Williams in Proc Soc Exp Biol & Med 99 632-633, 1958
Result: 19.5% lifespan increase in a longlived mouse strain (C57).
Favorable Effects of Pyridoxine HCl on the aging process by Lindseth K,
Dictor M & Miquel J in AGE 5(4), 143, 1968
Result: 11% total lifespan increase in a longlived strain (C57BL6J), even
though only applied after 18 months (late middle age for mice).
The Effect of Yeast Nucleic Acid on the Survival Time of 600-Day-Old Albino
Mice by TS Gardner, Journal of Gerontology 3(?) (1946), pages 445-452
Result: 16% lifespan increase
Composition and Biological Activity of Chromium-Pyridine Carboxylate
Complexes by GW Evans and DJ Pouchnik, Journal of Inorganic Biochemistry 49,
pg 177-187 (1993). This describes the action of dietary chromium picolinate
on inhibiting glycation in rodents as they aged. Early indications of the
lifespan increase (from the above experiment) were reported at the 22nd
American Aging Association conference (Oct 1992), after the paper was
submitted (March 1992) for publication, with further details in Chromium
Picolinate by GW Evans ISBN 0895299119
See also The Longevity Factor: Chromium Picolinate by RA Passwater, ISBN
0879836199
Result: 27% lifespan increase in rats
Cheers,
Michael C Price
Steve Harris
<870a5d01.02032...@posting.google.com>...
>
>Moderation in all things. But won't one man's high dose be another's
>optimum level? Some people benefit more from high folate levels than
>others due to a genetic lack of some enzyme or other (that was in one
>of last month's theads.)
Yes, that also is true of thiamin (only a subgroup of non-thifty
metabolizers get alcoholic thiamin-deficient encelphalopathy). And it is,
as you say, probably a general rule.
This is one of the nice things about vitamins with a range of 100 fold more
more between RDA and toxicity. This leaves you plenty of room to supplement
way over DRI levels, but still well short of what's likely to get you into
trouble.
Alas, yes.
SBH
Max Watt
...... That's it. Claims for a
> specific nutritional need for gamma-E or tocotrienols rest on test tube
> science or shaky post-hoc epidemiology, all of which are always insecure, to
> say the least. Frankly I don't believe them, due to the gold-standard
> semi-synthetic diet life span study results.
>
Not everyone agrees with you:
1: Am J Clin Nutr 2001 Dec;74(6):714-22
gamma-tocopherol, the major form of vitamin E in the US diet, deserves more
attention.
Jiang Q, Christen S, Shigenaga MK, Ames BN.
University of California, the Department of Molecular and Cell Biology,
Berkeley, USA.
gamma-tocopherol is the major form of vitamin E in many plant seeds and in the
US diet, but has drawn little attention compared with alpha-tocopherol, the
predominant form of vitamin E in tissues and the primary form in supplements.
However, recent studies indicate that gamma-tocopherol may be important to human
health and that it possesses unique features that distinguish it from
alpha-tocopherol. gamma-Tocopherol appears to be a more effective trap for
lipophilic electrophiles than is alpha-tocopherol. gamma-Tocopherol is well
absorbed and accumulates to a significant degree in some human tissues; it is
metabolized, however, largely to
2,7,8-trimethyl-2-(beta-carboxyethyl)-6-hydroxychroman (gamma-CEHC), which is
mainly excreted in the urine. gamma-CEHC, but not the corresponding metabolite
derived from alpha-tocopherol, has natriuretic activity that may be of
physiologic importance. Both gamma-tocopherol and gamma-CEHC, but not
alpha-tocopherol, inhibit cyclooxygenase activity and, thus, possess
antiinflammatory properties. Some human and animal studies indicate that plasma
concentrations of gamma-tocopherol are inversely associated with the incidence
of cardiovascular disease and prostate cancer. These distinguishing features of
gamma-tocopherol and its metabolite suggest that gamma-tocopherol may contribute
significantly to human health in ways not recognized previously. This
possibility should be further evaluated, especially considering that high doses
of alpha-tocopherol deplete plasma and tissue gamma-tocopherol, in contrast with
supplementation with gamma-tocopherol, which increases both. We review current
information on the bioavailability, metabolism, chemistry, and nonantioxidant
activities of gamma-tocopherol and epidemiologic data concerning the relation
between gamma-tocopherol and cardiovascular disease and cancer.
Publication Types:
Review
Review, Tutorial
PMID: 11722951
Steve Harris
news:<a7itka$aeq$1...@slb3.atl.mindspring.net>...
>...... That's it. Claims for a
>> specific nutritional need for gamma-E or tocotrienols rest on test tube
>> science or shaky post-hoc epidemiology, all of which are always insecure,
to
>> say the least. Frankly I don't believe them, due to the gold-standard
>> semi-synthetic diet life span study results.
>>
>
>Not everyone agrees with you:
Yes, I'm aware of this review. My response is <yawn>. Retrospective
epidemiology is why we do intervention trials. But you will remember the
story of beta carotene and lung cancer.
--
Steve Harris
michaelprice wrote in message ...
>Steve Harris:
>> You've have much the same body load (stores) of vitamin C if you ate 6
>> oranges a day as if you ate one. That's the point. It's an S-shaped
>> (sigmoidal) curve and you get 80 or 90% of the body stores from 100 mg of
>> vitamin C a day as if you eat 2 grams.
>
>Me:
>> Have you a reference for that?
>
>And a further thought. Over what time-scales where the experiments which
>Steve bases his conclusions on? It takes the human body years to fully
>respond to increased vitamin C intake. I quote
>
>"Vitamin C supplementation [500 mg.day] elevated plasma total ascorbate
>level
>by 30.1% (P:=0.043) in 12 months and
>by 91.1% (P:=0. 001) in 36 months"
You're kidding us, right? This is a study comparing groups of 11 and 12
people with each other (wow) which small n's cause them grief from the
beginning. Their placebo group starts with vitamin C levels of 60 +/-20 and
treatment group starts with levels of 80+/- 17, so the randomization hasn't
even started with comparable groups. After which the study finds results
that nobody else has gotten (see the MRC/BHF Heart protection study with
groups 30 times larger). It obviously has severe methodologic problems, like
not doing simultaneous sample analysis against baseline time zero, and gets
the expected drift from that (and deserves it). As a result it reports
several results which aren't credible-- for example the finding that placebo
group C levels regress toward the mean by going *down* 22 mg/dL in the first
year, then don't change after that (right). And the vitamin C group goes up
hardly at all the first year (+1.5) then zooms up at year 3 (+52). The word
for all this in groups of 12 people is "noise." It doens't mean we should
all rethink our idea of nutrition-- this is just a plain bad study with bad
data.
michaelprice
critique accepted - a flawed and noisey experiment.
Cheers,
Michael C Pricenews:a7jutd$4c5$1...@slb3.atl.mindspring.net...
Tom Matthews
>
>> Max Watt wrote in message
>> <870a5d01.02032...@posting.google.com>...
>>
>>
>>> Maybe that's why vitamin E doses of > 200 mg daily appear to be
>>> counterproductive
>>>
>>
>>
>> More likely it's exactly what we've been talking about. Vitamin E
>> has a U shaped effect on the immune system. Some improves your
>> immune function. Take too much and you sop up enough radicals to
>> actually begin to degrade response again (ie, it's anti-inflammatory
>> and immune suppressive). Again, inflammation and a better immune
>> response are closely related-- you don't get to willy-nilly turn up
>> one without effecting the other. There's no free lunch, and high dose
>> vitamin E is no exception.
>
> "more likely". Not only do the various E vitamers have seriously
> different effects, but there is excellent evidence to support their
> interdependence (not to mention their relationships with other
> vitamins and nutrients).
>
> COMMENT:
>
>
> I think "interdependence" is a strong word and probably a bad and misleading
> word
I disagree. When taking one E vitamer (alpha tocopherol) leads to a decrease
in endogenous levels of another E vitamer (gamma tocopherol), particularly in
compartments which depend on gamma tocopherol to do a certain job which alpha
tocopherol cannot replace, then I maintain "interdependence" is an accurate
term which is neither "bad" nor "misleading".
> for lack of total pharmacokinetic and pharmacodynamic independence.
You will have to explain how this relates to any "bad and misleading" use.
You can't read my mind (you constantly misrepresent me), and I certainly
cannot read yours.
> Very few things have total pharmacologic independence, and good examples are
> interactions between metabolism of numerous man-made drugs and various
> nutrients. Levels of some go up, others down when the vitamin is given in
> large amounts.
Of course. Your statement merely strengthens my own argument.
> None of which mean in the least that evolution has designed
> in some "interdependence" of these things
Now just *where* did I state or imply that it did?
> -- obviously for man-made drugs this is not the case.
Do you derive pleasure from stating the obvious, or do you do so because
you believe it causes readers to find your arguments more acceptable?
Either something is truly obvious to all and should not be stated or it
is *not* obvious to some and *should* be stated without insulting those
people by calling it obvious.
> But similar such findings are used to support supposed
> interdependence of E vitamers. That's bad reasoning.
No. Do not make the mistake of imputing to me reasoning which I did not
use! Besides, yours is the "bad reasoning" here.
To place everything in the context of evolution, as if it were some
"God" which has purposefully designed us is what is "bad reasoning".
Certainly, blind evolution and the spontaneous order of nature is
a wondrous thing and has created a highly effective and incredibly
complex human machine, but that does not imply that it is best possible
even in terms of its current operating mechanisms.
Personally, I never use evolution to argue one way or the other, since I
don't really care what evolution did or did not "do".
Actually, evolution did not "do" anything in the context of the correct
meaning of "do" - neither has evolution "designed in" anything in the
context of the proper usage of the word "design").
> There is an alpha tocopherol binding protein which picks this vitamer up
> preferentially, suggesting that this is the one the body prefers.
I don't agree that is any clear implication at all. For one thing, for it
to have any clear meaning, you would have to accurately define in detail
what you mean by "body prefers".
> There is NO evidence that the body needs any other vitamer.
This is incorrect. A PubMed search with gamma tocopherol + nitric oxide
yields the following beneficial effects of gamma tocopherol most of which
are greater than for alpha tocopherol.
1: Nitric Oxide 2002 Mar;6(2):221-227
The Nitration Product 5-Nitro-gamma-tocopherol Is Increased in the Alzheimer
Brain.
Williamson KS, Prasad Gabbita S, Mou S, West M, Pye QN, Markesbery WR, Cooney
RV, Grammas P, Reimann-Philipp U, Floyd RA, Hensley K.
Free Radical Biology and Aging Research Program, Oklahoma Medical Research
Foundation, 825 NE 13th Street, Oklahoma City, Oklahoma
Oxidative stress and quasi-inflammatory processes recently have been recognized
as contributing factors in the pathogenesis of Alzheimer's disease (AD).
Reactive nitrating species have specifically been implicated in AD based on
immunochemical and instrumental detection of nitrotyrosine in AD brain protein.
The significance of lipid-phase nitration has not been investigated in AD. This
study documents a significant two- to threefold increase in the lipid nitration
product 5-nitro-gamma-tocopherol in affected regions of the AD brain as
determined by high-performance liquid chromatography with electrochemical
detection. In a bioassay to compare the relative potency of alpha-tocopherol and
gamma-tocopherol against nitrative stress, rat brain mitochondria were exposed
to the peroxynitrite-generating compound SIN-1. The oxidation-sensitive Kreb's
cycle enzyme alpha-ketoglutarate dehydrogenase was inactivated by SIN-1, in a
manner that could be significantly attenuated by gamma-tocopherol (at <10
&mgr;M) but not by alpha-tocopherol. These data indicate that nitric
oxide-derived species are significant contributors to lipid oxidation in the AD
brain. The findings are discussed in reference to the neuroinflammatory
hypothesis of AD and the possible role of gamma-tocopherol as a major
lipid-phase scavenger of reactive nitrogen species. (C)2001 Elsevier Science
(USA).
PMID: 11890747 [PubMed - as supplied by publisher]
2: Biochem Biophys Res Commun 2000 Oct 22;277(2):334-40
gamma-tocopherol partially protects insulin-secreting cells against functional
inhibition by nitric oxide.
Sjoholm A, Berggren PO, Cooney RV.
Cancer Research Center of Hawaii, Molecular Carcinogenesis Program, University
of Hawaii at Manoa, 1236 Lauhala Street, Honolulu, Hawaii, 96813-2424, USA.
a...@ehk.ks.se
Preceding the onset of type 1 diabetes mellitus, pancreatic islets are
infiltrated by macrophages secreting interleukin-1beta (IL-1beta) which induces
beta-cell apoptosis and exerts inhibitory actions on islet beta-cell insulin
secretion. IL-1beta seems to act chiefly through induction of nitric oxide (NO)
synthesis. Hence, IL-1beta and NO have been implicated as key effector molecules
in type 1 diabetes mellitus. In this paper, the influence of endogenously
produced and exogenously delivered NO on the regulation of cell proliferation,
cell viability and discrete parts of the stimulus-secretion coupling in
insulin-secreting RINm5F cells was investigated. Because vitamin E may delay
diabetes onset in animal models, we also investigated whether tocopherols may
protect beta-cells from the suppressive actions of IL-1 and NO in vitro. To this
end, the impact of NO on insulin secretory responses to activation of
phospholipase C (by carbamylcholine), protein kinase C (by phorbol ester),
adenylyl cyclase (by forskolin), and Ca(2+) influx through voltage-activated
Ca(2+) channels (by K(+)-induced depolarization) was monitored in culture after
treatment with IL-1beta or by co-incubation with the NO donor spermine-NONOate.
It was found that cell proliferation, viability, insulin production and the
stimulation of insulin release evoked by carbamylcholine and phorbol ester were
impeded by IL-1beta or spermine-NONOate, whereas the hormone output by the other
secretagogues was not altered by NO. Pretreatment with gamma-tocopherol (but not
alpha-tocopherol) afforded a partial protection against the inhibitory effects
of NO, whereas specifically inhibiting inducible NO synthase with
N-nitro-L-arginine completely reversed the IL-1beta effects. In contrast,
inhibiting guanylyl cyclase with ODQ (1H-[1,2,
4]oxadiazolo[4,3-alpha]-quinoxaline-1-one) or blocking low voltage-activated
Ca(2+) channels with NiCl(2) failed to influence the actions of NO. In
conclusion, our data show that NO inhibits growth and insulin secretion in
RINm5F cells, and that gamma-tocopherol may partially prevent this. The results
suggest that phospholipase C or protein kinase C may be targeted by NO. In
contrast, cGMP or low voltage-activated Ca(2+) channels appear not to mediate
the toxicity of NO in these cells. These adverse effects of NO on the beta-cell,
and the protection by gamma-tocopherol, may be of importance for the development
of the impaired insulin secretion characterizing type 1 diabetes mellitus, and
offer possibilities for intervention in this process. Copyright 2000 Academic
Press.
PMID: 11032727 [PubMed - indexed for MEDLINE]
3: Proc Natl Acad Sci U S A 2000 Oct 10;97(21):11494-9
gamma-tocopherol and its major metabolite, in contrast to alpha-tocopherol,
inhibit cyclooxygenase activity in macrophages and epithelial cells.
Jiang Q, Elson-Schwab I, Courtemanche C, Ames BN.
Division of Biochemistry and Molecular Biology, University of California,
Berkeley, CA 94720, USA.
Cyclooxygenase-2 (COX-2)-catalyzed synthesis of prostaglandin E(2) (PGE(2))
plays a key role in inflammation and its associated diseases, such as cancer and
vascular heart disease. Here we report that gamma-tocopherol (gammaT) reduced
PGE(2) synthesis in both lipopolysaccharide (LPS)-stimulated RAW264.7
macrophages and IL-1beta-treated A549 human epithelial cells with an apparent
IC(50) of 7.5 and 4 microM, respectively. The major metabolite of dietary
gammaT, 2,7,8-trimethyl-2-(beta-carboxyethyl)-6-hydroxychroman (gamma-CEHC),
also exhibited an inhibitory effect, with an IC(50) of approximately 30 microM
in these cells. In contrast, alpha-tocopherol at 50 microM slightly reduced
(25%) PGE(2) formation in macrophages, but had no effect in epithelial cells.
The inhibitory effects of gammaT and gamma-CEHC stemmed from their inhibition of
COX-2 activity, rather than affecting protein expression or substrate
availability, and appeared to be independent of antioxidant activity. gamma-CEHC
also inhibited PGE(2) synthesis when exposed for 1 h to COX-2-preinduced cells
followed by the addition of arachidonic acid (AA), whereas under similar
conditions, gammaT required an 8- to 24-h incubation period to cause the
inhibition. The inhibitory potency of gammaT and gamma-CEHC was diminished by an
increase in AA concentration, suggesting that they might compete with AA at the
active site of COX-2. We also observed a moderate reduction of nitrite
accumulation and suppression of inducible nitric oxide synthase expression by
gammaT in lipopolysaccharide-treated macrophages. These findings indicate that
gammaT and its major metabolite possess anti-inflammatory activity and that
gammaT at physiological concentrations may be important in human disease
prevention.
PMID: 11005841 [PubMed - indexed for MEDLINE]
4: J Cardiovasc Pharmacol Ther 1999 Oct;4(4):219-226
Relative Effects of alpha- and gamma-Tocopherol on Low-Density Lipoprotein
Oxidation and Superoxide Dismutase and Nitric Oxide Synthase Activity and
Protein Expression in Rats.
Li D, Saldeen T, Romeo F, Mehta JL.
Department of Medicine, University of Florida, Gainesville, Florida
BACKGROUND: Increasing evidence suggests that vitamin E prevents the progression
of atherosclerosis by inhibiting platelet aggregation, monocyte adhesion, and
improving plaque stability and vasomotor function. Recently, controversy has
arisen as to the relative effects of alpha- and gamma-tocopherol in modulating
some mediators of atherosclerosis. METHODS AND RESULTS: We examined the effects
of alpha- and gamma-tocopherol on constitutive nitric oxide synthase (cNOS) and
superoxide dismutase (SOD) activity and protein expression in rats.
Sprague-Dawley rats were fed regular chow or chow mixed with alpha- or
gamma-tocopherol (100 mg/kg/day) for 7 to 10 days. Plasma alpha- and
gamma-tocopherol levels, low-density lipoprotein (LDL) oxidation, and cNOS and
SOD activity and protein expression were measured. Plasma alpha-tocopherol
levels were significantly increased (eP <.01 vs control), but gamma-tocopherol
levels fell (P <.01 vs control) in rats fed alpha-tocopherol. Plasma
gamma-tocopherol levels were increased (P <.01 vs control), and alpha-tocopherol
levels did not change in rats fed gamma-tocopherol. Both alpha- and
gamma-tocopherol feeding decreased the rate of LDL oxidation induced by phorbol
12-myristate 13-acetate (PMA)-stimulated leukocytes (P <.01 vs control). Both
alpha- and gamma-tocopherol increased SOD activity in plasma and arterial
tissues as well as Mn SOD and Cu/Zn SOD protein expression in arterial tissues
(all P <.01 vs control). gamma-Tocopherol was more potent than alpha-tocopherol
in all these effects (P <.05). Both a- and gamma-tocopherol increased NO
generation and cNOS activity (all P <.05 vs control). However, only
gamma-tocopherol increased cNOS protein expression. CONCLUSIONS: These
observations indicate that whereas both alpha- and gamma-tocopherol exert
important effects on determinants of oxidationand vasomotor function, effects of
dietary gamma-tocopherol supplementation in vivo are less pronounced than those
of gamma-tocopherol supplementation.
PMID: 10684543 [PubMed - as supplied by publisher]
5: FEBS Lett 1998 Feb 27;423(3):297-301
Erratum in:
FEBS Lett 1998 Jul 10;431(1):128
Interaction of peroxynitrite with carotenoids and tocopherols within low density
lipoprotein.
Pannala AS, Rice-Evans C, Sampson J, Singh S.
Department of Pharmacy, King's College, University of London, Chelsea, UK.
Peroxynitrite is a powerful oxidising and nitrating agent generated in vivo by
the combination of nitric oxide and superoxide. Previous studies have shown that
on exposure to peroxynitrite, low density lipoprotein (LDL) is modified
resulting in both a time- and concentration-dependent change to lipid and
protein components. The present investigation highlights the reaction between
carotenoids and tocopherols, present within the lipophilic phase of LDL, and
peroxynitrite at varying concentrations. It was observed that the carotenoids
were consumed by a significantly greater proportion than that of the tocopherols
with lycopene (87.2 +/- 11%) being more reactive than beta-carotene (68.2 +/-
5.8%) when exposed to peroxynitrite (50 microM) for 1 min. Among the
tocopherols, alpha-tocopherol (54.9 +/- 20.2%) was more extensively depleted
than gamma-tocopherol (14.7 +/- 1.09%) at peroxynitrite concentration of 500
microM. It was also observed that peroxynitrite, unlike copper ions, does not
lead to significant peroxidation of LDL as determined by the formation of
conjugated dienes and thiobarbituric acid-reactive substances.
PMID: 9515727 [PubMed - indexed for MEDLINE]
6: Nutr Rev 1997 Oct;55(10):376-8
gamma-Tocopherol: an efficient protector of lipids against nitric
oxide-initiated peroxidative damage.
Wolf G.
Department of Nutritional Sciences, University of California, Berkeley 94720,
USA.
Nitric oxide released by macrophages during inflammation reacts with active
oxygen to form peroxynitrite. Peroxynitrite nitrates protein and peroxidizes
lipids. gamma-Tocopherol traps peroxynitrite and is more effective than
alpha-tocopherol in protecting lipids against such peroxidation.
Publication Types:
Review
Review, Tutorial
PMID: 9354084 [PubMed - indexed for MEDLINE]
7: Free Radic Biol Med 1995 Sep;19(3):259-69
Products of gamma-tocopherol reaction with NO2 and their formation in rat
insulinoma (RINm5F) cells.
Cooney RV, Harwood PJ, Franke AA, Narala K, Sundstrom AK, Berggren PO, Mordan
LJ.
Cancer Research Center of Hawaii, Cancer Etiology Program, Honolulu 96813, USA.
gamma-Tocopherol, commonly found in seed oils, is the major tocopherol in the
U.S. diet, is superior to alpha-tocopherol in preventing neoplastic
transformation, and demonstrates unique reactivity toward NO2. This article
describes the products of reaction between gamma-tocopherol and low
concentrations of gaseous nitrogen dioxide (NO2), as well as their endogenous
formation in NO-producing RINm5F cells. gamma-Tocopherol in hexane reacts with
NO2 to yield two products identified as
2,7,8-trimethyl-2(4,8,12-trimethyltridecyl)-5,6-chromaquinone++ +, "tocored,"
and 2,7,8 trimethyl-2(4,8,12-trimethyltridecyl) 5-nitro, 6-chromanol,
"tocoyellow." Physical data for these two compounds and reaction characteristics
are described. The formation of tocored is consistent with a proposed mechanism
of gamma-tocopherol-mediated reduction of NO2 to NO involving initial reaction
by NO2 at the C-5 position to form an intermediate nitrite ester tocopheryl
radical, which then reacts internally to release NO and form 5,6 epoxy
gamma-tocopherol. Tautomerization and further oxidation of the latter
intermediate by NO2 yields tocored as the main product observed. The reaction of
gamma-tocopherol with NO2 to form NO occurs independently of light, whereas
alpha-tocopherol requires light to generate NO from NO2. gamma-Tocopherol and
aminoguanidine, an NO synthase inhibitor, were superior to alpha-tocopherol in
preventing RINm5F cell toxicity induced by Interleukin-1 beta (IL-1 beta). Both
tocored and tocoyellow were observed to form in RINm5F cells loaded with
gamma-tocopherol and producing NO constitutively, although a consistent increase
in these products as a result of induced NO synthesis was not observed.
PMID: 7557540 [PubMed - indexed for MEDLINE]
8: Proc Natl Acad Sci U S A 1993 Mar 1;90(5):1771-5
Gamma-tocopherol detoxification of nitrogen dioxide: superiority to
alpha-tocopherol.
Cooney RV, Franke AA, Harwood PJ, Hatch-Pigott V, Custer LJ, Mordan LJ.
Cancer Research Center of Hawaii, University of Hawaii, Honolulu 96813.
In the vitamin E group, alpha-tocopherol is generally considered to be the most
potent antioxidant with the highest vitamin bioactivity, yet gamma-tocopherol is
produced in greater amounts by many plants and is the principal tocopherol in
the United States diet. This report describes a fundamental difference in the
chemical reactivities of alpha-tocopherol and gamma-tocopherol with nitrogen
dioxide (NO2), which leads to the formation of a nitrosating agent from
alpha-tocopherol, but not from gamma-tocopherol. Nitric oxide (NO) is a major
product of the reaction of gamma-tocopherol with NO2, while alpha-tocopherol
reacts with NO2 to form an intermediate tocopheroxide analogue. The biological
significance of gamma-tocopherol is suggested by limited epidemiological data as
well as the observation that it is a more potent inhibitor than alpha-tocopherol
of neoplastic transformation during the postinitiation phase in
3-methylcholanthrene-treated C3H/10T1/2 murine fibroblasts. This latter property
suggests the superiority of gamma-tocopherol in a mammalian biological assay and
a role for endogenous NO production in promotion of neoplastic transformation.
PMID: 8446589
There are many others for effect other than those that are related to nitric oxide.
I can't believe you are ignorant of this literature.
> There are no deficiency
> symptoms or signs or any other problems known in animals not getting the
> other vitamers.
How do you know that and how do you know it is true for human animals? What kind
of diet contains zero gamma tocopherol?
> Life span studies done by myself and many other researchers
> show perfectly normal life span studies with alpha tocopherol primarly (and
> for that matter, these studies have classically been done with the dl,dl,dl
> 8-isomer mix, only one of which is found in nature).
Again, by what measures are they normal?
Are all mortality rates for each disease type the same?
Are the mean lifespans identical?
Finally, humans die of many more and different causes than lab mice do!
> Possibly the animals
> also get some gamma from the corn oil typically used in them as fat source,
> but it's not much.
It is some, and certainly does not show that animals can live entirely without
gamma tocopherol.
> The life span controls for these studies are those
> historical studies in the pre-chow era, in which animals got mixed food
> diets, where the E is mostly gamma-E. Life span's weren't any better, and
> were usually worse.
If you didn't do controls within the very same study, then the studies are not
worth much!
In any case this does not refute my points because:
1) The studies were not done under the exact same conditions.
2) Lab animals do not get the multitude of diseases and debilitating conditions
which humans do.
3) A mice cannot and does not always let you know when it is in a diseased state
which is not necessarily terminal.
4) I am not merely talking about life span here. Life quality in terms of energy
and productive capacity are also important for humans.
> We know from the reproductive studies that any active E vitomer is able to
> substitute for any other, to the limit of delectability of pathology.
Reproductive studies don't necessarily say anything about adult needs or benefits.
> One
> study has been done in which animals were raised for 3 generations on
> nothing but gamma-E. They did fine, but apparently were able to convert
> some gamma to alpha-E.
Thanks for that piece of information. I had wondered if that might be true.
However, this conversion ability (if humans have it) may decline with age.
> Again this suggests that alpha-E is what the body
> prefers (for storage if for nothing else).
Again we see the use of a misleading, consciousness implying phrase
("body prefers") for something which has no thought behind it.
Besides how does it suggest any such thing as that "alpha is most
important"? All that it suggests is that the lab animals need some alpha.
It also does not preclude that they need some gamma also and perhaps
possess a mechanism to convert alpha to gamma if they do not get enough
in their diet.
> That's it. Claims for a
> specific nutritional need for gamma-E or tocotrienols rest on test tube
> science or shaky post-hoc epidemiology,
This is simply your *opinion* because you disagree with the alternative
(for whatever ulterior motive I do not know).
> all of which are always insecure, to say the least.
No more so, IMO, than the studies which you have talked about (although for
different reasons).
> Frankly I don't believe them, due to the gold-standard
> semi-synthetic diet life span study results.
Frankly, I don't care *what* you "believe"! I am only interested
in the facts you know and what you *think*.
>>Of course, "there is no free lunch"! One cannot willy-nilly simply take
>>large doses of any one particular vitamin or nutrient without some
>>downsides! *Everything* has a U shaped dose/effect curve. To use a
>>phrase that I learned from you: "the dose makes the poison". However,
>>this does not preclude the possibility of beneficially taking a selected
>>combination of vitamins and nutrients at above food obtainable levels,
>>by intelligently reading the research and using it to guide one's
>>choices. To think that such is not possible (as you appear to do) is to
>>embrace an extremely negative, pessimistic and cynical world-view (which
>>you again appear to do - perhaps because of your own advancing age and
>>declining physical condition - I hardly recognized your new picture.
>>BTW, a little CR would help you a lot.).
>>
>
> No, now, ad hominem.
I really was not making any ad hominem. I truly am trying to understand
your cyncial, pessimitic world view which seems now to be considerably
worse than when I first met and worked with you ten years ago.
> Yes, nearing age 45 I've certainly lost my boyish
> charm (unlike you, "Tom," who at age 45 were no doubt still being mistaken
> for 25. Not).
I never said anything about myself. I did not look after myself well healthwise
before age 45 (although I had no major problems), but I have not aged nearly as
much in the last 20 years as I did in the prior 20.
> Today's newsflash: that tends to happen to us humans (take a
> look at Bill Gates, Michael J. Fox, Pearson and Shaw, and basically most
> people of average genetics who haven't had plastic surgery).
But for someone who has your in-depth knowledge to let yourself get so overweight,
with all the damage it can do (much of it irreversible) is truly intolerable.
> No, I don't like it. And yes, in fact, I am on a diet.
You need a total food lifestyle change. A "diet" is worse than useless.
> And no, I refuse to dye my hair
> or have a facelift. Graying hair is not fixable with nutrition; the
> middle-age spread of course is.
Better still, it shouldn't have been allowed to happen. Even I knew that, way
back then. And my father, brother and sister were all overweight (my mother
died early of ALS).
> But it's also mostly cosmetic and low
> levels. My physical condition is fine.
Ha! This from someone who is supposed to be an expert on these things! I'll
match all my physiological parameters against you any day and I am 20 years older!
> I know because I'm not dead, having
> recently subjected my body to learning scuba. This is not tropical
> paddling, but diving in the West coast Pacific, to depths below 100 ft, in
> water at depth around 60 F (15 C).
At 40+ I also learned scuba and dived in much colder Ontario waters (5'C -
though not quite so deep). And I did not have any excess fat to keep me warm.
> Lots of fun, but (by the way) a place
> where you're glad for every pound of extra fat-- it's not going to be nearly
> as much fun when I'm skinnier.
That is what wet-type diving suits are for.
> Caloric restriction (CR) may be great if you
> want to sit in a nice climate-controlled lab basement or a sealed controlled
> experiment in some warm place like Biosphere II. However, In other places--
> on top of a mountain in the snow, under a lot of cold water in the Pacific,
> or with a nasty infection-- you may well pay a price for CR that you hadn't
> counted on.
One does not *need* to do such things in our civilized world. I am the first
to agree that if your life or priorities require it, then you should not be on
CR. However, you are then saying, in effect, that you are not very interested
in extending your life.
> That is why I'm particularly watching you restricted Canucks--
> the first one of you that crumps from infection is going to be editorialized
> by moi.
There are such things as warm clothes, you know.
> If I die first of a heart attack you can do the same for me, but
> don't hold your breath-- my numbers are perfect.
So are mine and I don't get infections. But there are many other ways for
an overweight person to debilitate faster than I am besides a heart attack.
>>*That* is what we are arguing may well be possible today and, in fact,
>>has some reasonable amount of evidence in its favor. And neither you nor
>>anyone else can express more than an *opinion* that we are wrong.
>>
>
> That it's my "opinion" goes without saying. But burden of evidence is on
> you, not me.
I am not sure why you think this is true. I am not trying to imply any proof.
All that I am trying to do is show a reasonable weight of evidence that
certain modes of dietary and other behaviors have some reasonable chance of
improving my quality of life, delaying my senescence and possibly increasing
my life span. Since you and others have no better method of causing these
things to happen, I will continue to do as I am and I urge others who truly
desire these same benefits to do likewise.
It is a little like cryonics, Steve. It may have little chance to work, but
all alternatives are worse.
> I've given you my reasoning. The gold standard in experimental
> gerontology
Relative to others, maybe a "gold standard", but in absolute terms of relevancy
and value no more than a "lead standard" at best.
> - failing actual human trial results--
Totally flawed trials, which were almost bound to fail (if not purposefully
designed to do so).
> is mammalian life span studies using long-lived strains.
1) Rodents are not humans.
2) Humans don't live in cages and eat lab chow.
3) Rodents die of a different profile of conditions than do humans.
4) Even more so do rodents have a vastly different profile of disabling conditions.
5) This is mainly because rodents do not live long enough to be good models
for many of the pathological processes which cause decline with age in
humans and which disable or kill them.
6) Specifically, the pathological damage accumulation which takes decades
to occur in humans and likely makes much of the difference between a
20 year old and an 80 year old, has no comparative model in rodents.
In short, though they may be what we have mostly used for life span and
life quality studies (mainly because they are most easily worked with),
rodents are, in fact, a very poor model of human aging.
Yes, rodents have basically similar biochemical processes and can thus
be used to study these individual processes in isolation, but how these
processes interact to cause the animal to remain alive over a lifetime
is another thing entirely and is totally different between rodents and humans!
> Vitamin-wise, they don't argue for your side, but mine.
For the reaons that I have given, they don't argue very strongly against it
either. OTOH, thousands of other types of studies showing a multitude of
benefits from various nutrients argue for strongly for it, IMO.
> So far as CR goes, rodent studies argue for your view in
> controlled conditions, and primate studies are on-going (too early to tell;
> biomarkers look good, but they too are being pampered). I think the jury's
> still out for the real world and humans. You may well be right.
The last two statements are the first "light" I have seen from the dark cloud that envelopes you.
> Or you may well be wrong.
I would rather die trying and wrong, than not try at all and die "naturally"!
> Again, I have little doubt that we're in for a lot of CR
> people dying of funny diseases, while all the while their compadres are
> saying "Well, if it wasn't for THAT freak thing, he'd have gotten to 150!"
This is one reason that I advocate only moderate CR for real world humans.
> But that's not the way it works. In the real world, there's a U-shaped
> survival curve for body mass index, too, and it's not where CR would
> predict.
The major problem is that the studies which produce data for that curve
do not take into account underlying pathologies which caused, or were
correlated with the low weight. These studies, therefore, have little
relevance to those who purposefully restrict caloric intake. To suggest
that they do is to reverse cause and effect.
> CR's advocates have a lot of explanation for that (ho hum
Insulting their explanations with a "ho hum" does nothing to refute them.
> -- maybe
> enough vitamins weren't being taken; that's what life-extenders ALWAYS say),
> but butt they remain ad-hoc apologias for now. I believe some of them, and
> others not.
Again, I don't really care what you "believe". I care only for facts and
rational arguments (what you *think*).
> I retain skepticism also. I've seen a lot of great theories in
> medicine go down the tubes, and others succeed. Which was going to succeed
> was by no means obvious, until the final results were in.
I certainly agree with these last statements. That is why I often have
little patience with all the theorizing which so many people do when there
is no one doing any testing of their conclusions.
Michael
"michaelprice" <michae...@ntlworld.com> wrote in message news:<KQKl8.5546$WP.11...@news2-win.server.ntlworld.com>...
> "Steve Harris" <sbha...@ix.RETICULATEDOBJECTcom.com> wrote in message
>
> > You've have much the same body load (stores) of vitamin C if you ate 6
> > oranges a day as if you ate one. That's the point. It's an S-shaped
> > (sigmoidal) curve and you get 80 or 90% of the body stores from 100 mg of
> > vitamin C a day as if you eat 2 grams.
>
> Have you a reference for that?
Since Steve never directly answered this, I will:
>
Proc Natl Acad Sci U S A 1996 Apr 16;93(8):3704-9
Vitamin C pharmacokinetics in healthy volunteers: evidence for a
recommended
dietary allowance.
Levine M, Conry-Cantilena C, Wang Y, Welch RW, Washko PW, Dhariwal KR,
Park JB,
Lazarev A, Graumlich JF, King J, Cantilena LR.
... Steady-state plasma and tissue concentrations were determined at
seven daily doses of vitamin C from 30 to 2500 mg.
Vitamin C steady-state plasma concentrations as a function of dose
displayed sigmoid kinetics. The steep portion of the curve occurred
between the 30- and 100-mg daily dose, the current RDA of 60 mg daily
was on the lower third of the curve, the first dose beyond the sigmoid
portion of the curve was 200 mg daily, and complete plasma saturation
occurred at 1000 mg daily.
Neutrophils, monocytes, and lymphocytes saturated at 100 mg daily and
contained
concentrations at least 14-fold higher than plasma.
Bioavailability was complete for 200 mg of vitamin C as a single dose.
No vitamin C was excreted in urine of six of seven volunteers until
the 100-mg dose.
At single doses of 500 mg and higher, bioavailability declined and the
absorbed amount was excreted. ...
PMID: 8623000
---
Am J Clin Nutr 1979 Mar;32(3):530-9
Steady-state turnover and body pool of ascorbic acid in man.
Kallner A, Hartmann D, Hornig D.
The time course of radioactivity in plasma and urine after oral
administration
of a single dose of (1-14C)ascorbic acid has been followed in healthy
nonsmoking
male volunteers. The investigation was carried out under steady state
conditions
with regard to ascorbic acid intake (30 to 180 mg/day). ...
It was found that the half-life of ascorbic acid was inversely related
to the dosage and that the pool could be increased to about 20 mg/kg
bodyweight by increasing the dosage. It was concluded that on a daily
intake of about 100 mg ascorbic acid this pool size would be reached
in 95% of the population.
PMID: 420145
In apparent confirmation of the optimality of such intake,
epidemiological data summarized in this review:
Carr AC, Frei B.
Toward a new recommended dietary allowance for vitamin C based on
antioxidant
and health effects in humans.
Am J Clin Nutr. 1999 Jun;69(6):1086-107. Review.
PMID: 10357726
... SEEM to show that increasing intake up to this range is
protective, while further intake is no more so. Hence, these Linus
Pauling Institute investigators suggest a new RDA, designed to
"optimally protect against" "cancer, cardiovascular disease, and
cataract" of 90-100 mg/day, except in those specifically exposed to
C-depleting circumstances such as smoking, pregnancy, and biological
old age.
-Michael
--
The terror attacks are explained -- but not justified -- by terror
created by US government foreign policy. From the cause, discern the
cure.
http://www.csmonitor.com/2001/0927/p1s1-wogi.htm
http://www.zmag.org/shalomhate.htm
http://www.public-i.org/excerpts_01_091301.htm
Michael
"michaelprice" <michae...@ntlworld.com> wrote in message news:<VF8n8.5541$Dr3.1...@news6-win.server.ntlworld.com>...
> Steve Harris:
> > The gold standard
> > in experimental gerontology- failing actual human trial results-- is
> > mammalian life span studies using long-lived strains. Vitamin-wise,
> > they don't argue for your side, but mine.
>
> Steve, can you please explain the deficiencies of these three experiments:
>
> Effect of pantothenic acid on the longevity of mice by Richard B Pelton and
> Roger J Williams in Proc Soc Exp Biol & Med 99 632-633, 1958
> Result: 19.5% lifespan increase in a longlived mouse strain (C57).
>
> Favorable Effects of Pyridoxine HCl on the aging process by Lindseth K,
> Dictor M & Miquel J in AGE 5(4), 143, 1968
> Result: 11% total lifespan increase in a longlived strain (C57BL6J), even
> though only applied after 18 months (late middle age for mice).
>
> The Effect of Yeast Nucleic Acid on the Survival Time of 600-Day-Old Albino
> Mice by TS Gardner, Journal of Gerontology 3(?) (1946), pages 445-452
> Result: 16% lifespan increase
The problem with these 3 experiments, in the present context, is that
none of them actually show any extension of normal lifespan. The
normal av'g lifespan of mice which are not genetic fuckups, & which
are properly cared for (not raised in intrinsically life-shortening
environments, as shown by shortened av'g LS for their strain), is in
the 31 month (942 day) ballpark. The "extended" av'g LS of Pelton &
Williams' supplemented colony was just 660 days, with no extension in
their (also short) colony "max LS." Similar considerations hold for
the other experiments, above.
If I prove that I can extend the LS in a Brazillian community exposed
to Hg because of criminal gold refining practices by giving one group
of them succimer, but they STILL don't live, on average, as long as
normal, healthy folk not exposed to Hg, that's not evidence that
succimer supplementation is of benefit to the unexposed.
Additionally, the Lindseth experiment reported lower BW in the B6
group: crypto-CR is likely at play in the paltry pseudo-extension
observed.
>
> Composition and Biological Activity of Chromium-Pyridine Carboxylate
> Complexes by GW Evans and DJ Pouchnik, Journal of Inorganic Biochemistry 49,
> pg 177-187 (1993). This describes the action of dietary chromium picolinate
> on inhibiting glycation in rodents as they aged. Early indications of the
> lifespan increase (from the above experiment) were reported at the 22nd
> American Aging Association conference (Oct 1992), after the paper was
> submitted (March 1992) for publication, with further details in Chromium
> Picolinate by GW Evans ISBN 0895299119
Alas, (a) the results were never properly published; (b) the
supplemented group's low bodyweights suggests that it was crypto-CR,
not Cr, doing the trick, and (c) Steve himself found no such effect:
http://groups.google.com/groups?selm=79bs4b%24dfl%40dfw-ixnews3.ix.netcom.com&output=gplain
---------------------------------
> How much CrPic?
1 part in 10,000 as Cr. About 75 mg (75,000 mcg) Cr per day in
human
terms. 375 times the top "safe and effective" 200 mcg per day.
> Did the latter
>confirm Evans' curve-squaring?
Nope. Nor did the animals lose weight. However, all were
restricted by 10% anyway, and I didn't try it on fat ad libers.
-------------------------------------
Anderson et al also would appear to have demonstrated that CrPic
doesn't extend LS (tho' I agree this is argumentum ab silentio):
J Am Coll Nutr 1997 Jun;16(3):273-9
Lack of toxicity of chromium chloride and chromium picolinate in rats.
Anderson RA, Bryden NA, Polansky MM.
.,.. Harlan Sprague Dawley rats (4 weeks of age) were fed a stock diet
to which was added 0, 5, 25, 50 or 100 mg of Cr per kg of diet as
chloride or picolinate. ... There were no statistically significant
differences in body weight, organ weights or blood variables among all
the groups tested at 11, 17 and 24 weeks. Blood variables measured
were glucose, cholesterol, triglycerides, blood urea nitrogen, lactic
acid dehydrogenase, transaminases, total protein and creatinine.
Histological evaluation of the liver and kidney of control and animals
fed 100 mg/kg Cr as Cr chloride or picolinate also did not show any
detectable differences. ...
PMID: 9176835
That is: there is no evidence that any of these supplements will
extend LS in normal, healthy animals raised under proper (not
intrinsically life-shortening) conditions.
NB that Cr does not, apparently, improve glycemia (its putative
life-extending/CR-mimetic mechanism) in non-diabetics:
1: J Am Coll Nutr 2001 Aug;20(4):293-306
Effect of chromium supplementation and exercise on body composition,
resting metabolic rate and selected biochemical parameters in
moderately obese women following an exercise program.
Volpe SL, Huang HW, Larpadisorn K, Lesser II.
... Twelve weeks of 400 microg/day of chromium as a CP supplement did
not significantly affect body composition, RMR, plasma glucose, serum
insulin, plasma glucagon, serum C-peptide and serum lipid
concentrations or iron and zinc indices in moderately obese women
placed on an exercise program. The changes in serum total cholesterol
levels and TIBC were a result of the exercise program.
PMID: 11506057 [PubMed - indexed for MEDLINE]
J Gerontol A Biol Sci Med Sci 2000 May;55(5):M260-3
Effects of chromium picolinate supplementation on insulin sensitivity,
serum lipids, and body composition in healthy, nonobese, older men and
women.
Amato P, Morales AJ, Yen SS.
..... Chromium picolinate supplementation alone does not appear to
improve insulin sensitivity, serum lipids, or change body composition
in nonobese, healthy men and women of advanced age.
PMID: 10819315 [PubMed - indexed for MEDLINE]
---
Metabolism 1999 May;48(5):546-53
Effect of resistance training with or without chromium picolinate
supplementation on glucose metabolism in older men and women.
Joseph LJ, Farrell PA, Davey SL, Evans WJ, Campbell WW.
... High-dose Cr-pic supplementation had no effect on any measure of
glucose metabolism [fasting concentration or AUC for glucose, insulin,
or C-peptide] during R[esistance ]T[raining].
PMID: 10337851 [PubMed - indexed for MEDLINE]
---
Most studies also show no effect on weight loss, muscle gain, etc,
whether in young atheletes or old folks trying to recover some lost
muscle mass; and any such improvements might easily be the simple
result of correcting the increased excretion caused by exercise (ie a
correction of deficiency, not a pharmacological effect reproducible
thru' megadosing & applying to the population at large).
michaelprice
"Michael" <mik...@lycos.com> wrote in message
news:69779556.02032...@posting.google.com...
> All:
>
>> Effect of pantothenic acid on the longevity of mice by Richard B Pelton
>> and Roger J Williams in Proc Soc Exp Biol & Med 99 632-633, 1958
>> Result: 19.5% lifespan increase in a longlived mouse strain (C57).
>>
>> Favorable Effects of Pyridoxine HCl on the aging process by Lindseth K,
>> Dictor M & Miquel J in AGE 5(4), 143, 1968
>> Result: 11% total lifespan increase in a longlived strain (C57BL6J), even
>> though only applied after 18 months (late middle age for mice).
>>
>> The Effect of Yeast Nucleic Acid on the Survival Time of 600-Day-Old
>> Albino Mice by TS Gardner, Journal of Gerontology 3(?) (1946),
>> pages 445-452
>> Result: 16% lifespan increase
>
> The problem with these 3 experiments, in the present context, is that
> none of them actually show any extension of normal lifespan. The
> normal av'g lifespan of mice which are not genetic fuckups, & which
> are properly cared for (not raised in intrinsically life-shortening
> environments, as shown by shortened av'g LS for their strain), is in
> the 31 month (942 day) ballpark.
This assumes that the concept of a species LS has any relevance.
It hasn't. The raising of the species maximum lifespan by the
discovery (e.g. the "indy" gene) , or creation by selective breeding
(ala Michael Rose), of a longer-lived strain within a species invalidates
it as a meaningful yardstick.
> The "extended" av'g LS of Pelton & Williams' supplemented colony
> was just 660 days, with no extension in their (also short) colony
> "max LS."
I question the veracity of your "max LS" figures. According to Walford
(page 176, 120 yr diet) *NO* max LS figures were reported for the
Pelton & Williams work.
> Similar considerations hold for the other experiments, above.
I entertain similiar doubts for any unreferenced sources!
> Additionally, the Lindseth experiment reported lower BW in the B6
> group: crypto-CR is likely at play in the paltry pseudo-extension
> observed.
Since the B6 was administered in drinking water this is not plausible.
BTW I don't call 11% LE when treatment begins in late middle
age "paltry", but that's just a matter of "taste", I guess. :-)
>> Composition and Biological Activity of Chromium-Pyridine Carboxylate
>> Complexes by GW Evans and DJ Pouchnik, Journal of Inorganic
>> Biochemistry 49, pg 177-187 (1993). This describes the action of
>> dietary chromium picolinate on inhibiting glycation in rodents as they
>> aged. Early indications of the
>> lifespan increase (from the above experiment) were reported at the 22nd
>> American Aging Association conference (Oct 1992), after the paper was
>> submitted (March 1992) for publication, with further details in Chromium
>> Picolinate by GW Evans ISBN 0895299119
>
> Alas, (a) the results were never properly published; (b) the
> supplemented group's low bodyweights suggests that it was crypto-CR,
> not Cr, doing the trick, and (c) Steve himself found no such effect:
Steve's "controls" - for which criticism (a) applies!! - were on 10%
restriction. Tragic since CR improves glucose tolerance.
For (b) see B6 comments for my scepticism of crypto-CR
> Anderson et al also would appear to have demonstrated that CrPic
> doesn't extend LS (tho' I agree this is argumentum ab silentio):
Max age of rats = 24 weeks explains lack of LE or any detectable
effect!!!
The remaining CrPic counter-studies cited were not about LS.
Some studies show a benefit for diabetics, others don't. Obviously
more work needs to be done to clarify the issue.
(I'm not moved by the null studies which have screened out diabetic
and pre-diabetic subjects, since it is quite likely that the benefit of
CrPic is entirely due to the improvement (admitedly putative)
of glucose tolerance.)
Cheers,
Michael C Price
michaelprice
>
> "michaelprice" <michae...@ntlworld.com> wrote in message
news:<KQKl8.5546$WP.11...@news2-win.server.ntlworld.com>...
>> "Steve Harris" <sbha...@ix.RETICULATEDOBJECTcom.com> wrote in message
>>
>>> You've have much the same body load (stores) of vitamin C if you ate
>>> 6 oranges a day as if you ate one. That's the point. It's an S-shaped
>>> (sigmoidal) curve and you get 80 or 90% of the body stores from
>>> 100 mg of vitamin C a day as if you eat 2 grams.
>>
> > Have you a reference for that?
>
> Since Steve never directly answered this, I will:
>
> Proc Natl Acad Sci U S A 1996 Apr 16;93(8):3704-9
>
> Vitamin C pharmacokinetics in healthy volunteers: evidence for a
> recommended dietary allowance.
>
> Levine M, Conry-Cantilena C, Wang Y, Welch RW, Washko PW,
>
> ... Steady-state plasma and tissue concentrations were determined at
> seven daily doses of vitamin C from 30 to 2500 mg.
There's no evidence that this is anything but a single dose experiment,
which isn't allowing the body time to adjust to the higher vitamin C intake,
which the rebound effects suggests is physiologically significant.
The only work with vitamin C & excretion I can think off, off-hand,
which explicitly allowed a long acclimitisation period to the ascorbic
acid intake, is Michael Colgan's work, which found that the average
subject didn't excrete any ascorbic acid products until intake was in
the 2-3 grams / day range.
> In apparent confirmation of the optimality of such intake,
> epidemiological data summarized in this review:
>
> Carr AC, Frei B.
> Toward a new recommended dietary allowance for vitamin C
> based on antioxidant and health effects in humans.
> Am J Clin Nutr. 1999 Jun;69(6):1086-107. Review.
> PMID: 10357726
>
> ... SEEM to show that increasing intake up to this range is
> protective, while further intake is no more so. Hence, these Linus
> Pauling Institute investigators suggest a new RDA, designed to
> "optimally protect against" "cancer, cardiovascular disease, and
> cataract" of 90-100 mg/day, except in those specifically exposed to
> C-depleting circumstances such as smoking, pregnancy, and
> biological old age.
The above survey is not as definite as that. I quote from the summary:
"Therefore, we suggest that the RDA for vitamin C be doubled to 120 mg/d.
Even higher intakes of vitamin C, and possibly supplementation, may be
required to reduce cataract risk (Table 8), although the evidence is less
secure because of the limited number of studies. Furthermore, chronic
500-mg/d doses or acute 1-3-g doses of vitamin C significantly improve
vasoreactivity."
Cheers,
Michael C Price
Steve Harris
<4ABn8.18030$Dr3.2...@news6-win.server.ntlworld.com>...
>Steve's "controls" - for which criticism (a) applies!! - were on 10%
>restriction. Tragic since CR improves glucose tolerance.
Actually, it doesn't (at least in mice): you should see the glucose
tolerance curves in my 40% CR animals-- horrible (abstract is below, but it
really takes looking at the graphs to get the full impact). Being on severe
CR doesn't give you a pancreas with a lot of reserve (not surprisingly).
It's the average and fasting glucoses that are low in CR. 10% gives
intermediate fasting glucoses, and the best glucose tolerance to acute
challenge. Ad lib animals are pre-diabetic. Incidentally I did run some of
these on Cr picolinate for a while and got no glucose effect. I couldn't get
ANY effect of this stuff in my model on ANY parameter.
Thanks to Michael for answering the other parts of your question and doing a
lot of work for me. I will add only that the literature of gerontology is
litered with claims for life span improving properties of all kinds of
things: Vitamins C and E, DMAE, cysteine, cysteamine, BHT,
ethoxyquin, deprenyl, CoQ10, lots of other stuff. It proved to be
unrepeatable, by and large. I don't even completely believe my own results
until they've been confirmed; it's too easy to fool yourself in science.
There are also old reports from the 40's, 50's and 60's like the ones you
cite: never confirmed and there they sit. My guess is that if they were
repeatable they also would have been confirmed. Since they haven't, we can
ignore them. If you want to try repeating them yourself and maybe be
famous, be my guest.
Mech Ageing Dev 1994 Mar;73(3):209-21 Related Articles, Books, LinkOut
Serum glucose, glucose tolerance, corticosterone and free fatty acids during
aging in energy restricted mice.
Harris SB, Gunion MW, Rosenthal MJ, Walford RL.
Department of Pathology, University of California at Los Angeles 90024.
Energy restriction, the only method known to increase maximum life span in
laboratory animals, was used as a tool to test hypotheses regarding possible
mechanisms of aging. Serum glucose and corticosterone (CS) concentrations in
mice of a long-lived hybrid mouse strain, aged 7, 17, and 29 months, and on
50%, 80%, and 100% of ad libitum intake, were measured. Serum glucose and CS
concentrations were also measured in response to intraperitoneal (i.p.)
glucose challenge in mice at ages 7 and 29 months. Serum glucose and CS
concentrations were also measured at several time points over 36 h, to
assess their diurnal variation. There were no differences in single fasting
glucose concentrations in 7- and 29-month-old mice at the same degree of
energy restriction, but energy restriction decreased glucose concentrations.
Serum CS concentrations were generally increased restricted animals with
respect to fully fed ones. Average serum glucose concentrations were found
to be significantly decreased by dietary restriction. Glucose tolerance
curves were unchanged by age in ad libitum fed or 50% restricted animals,
but in 80% ad libitum groups, older animals showed evidence of decreased
glucose tolerance with respect to young animals. For each age, peak serum
glucose concentrations after i.p. glucose loading varied with degree of
energy restriction, with more severely restricted animals showing less
glucose tolerance. Average serum CS concentrations were elevated at 7 months
by restriction, especially at night and long after feeding, but we found no
differences with age or diet in average CS concentrations. Our serum glucose
results support the hypothesis that nonenzymatic glycation is
mechanistically involved in normal aging. Our serum CS results do not
support the hypothesis that CS contributes significantly to the
pathophysiology of normal aging in mice.
PMID: 8057691 [PubMed - indexed for MEDLINE]
michaelprice
> michaelprice wrote in message
> <4ABn8.18030$Dr3.2...@news6-win.server.ntlworld.com>...
>
>>Steve's "controls" - for which criticism (a) applies!! - were on 10%
>>restriction. Tragic since CR improves glucose tolerance.
>
> Actually, it doesn't (at least in mice): you should see the glucose
> tolerance curves in my 40% CR animals-- horrible (abstract is below,
> but it really takes looking at the graphs to get the full impact). Being
> on severe CR doesn't give you a pancreas with a lot of reserve
> (not surprisingly).
> It's the average and fasting glucoses that are low in CR. 10% gives
> intermediate fasting glucoses, and the best glucose tolerance to acute
> challenge. Ad lib animals are pre-diabetic. Incidentally I did run
> some of these on Cr picolinate for a while and got no glucose effect.
Old, young or both?
> I couldn't get ANY effect of this stuff in my model on ANY parameter.
Including insulin levels?
You really should publish since it is impossible to critique unpublished
word-of-mouth stuff.
> Thanks to Michael [R] for answering the other parts of your question
> and doing a lot of work for me. I will add only that the literature of
> gerontology is litered with claims for life span improving properties
> of all kinds of things: Vitamins C and E, DMAE, cysteine, cysteamine,
> BHT, ethoxyquin, deprenyl, CoQ10, lots of other stuff. It proved to be
> unrepeatable, by and large. I don't even completely believe my own results
> until they've been confirmed; it's too easy to fool yourself in science.
> There are also old reports from the 40's, 50's and 60's like the ones you
> cite: never confirmed and there they sit. My guess is that if they were
> repeatable they also would have been confirmed.
My guess is that they haven't been repeated because the B-vitamins, RNA
and minerals don't fit into the antioxidant / free-radical paradigm that has
been in vogue for so long. And also that they are unpatentable, so no
drug company funding.
I share Steve's view - correct me if wrong - that free radicals only play
a small part in aging at best. The most effective age retarders seem to
be dietary precursors to enzymatic cofactors, rather than the antioxidants
such as vitamins C and E, BHT & ethoxyquin
> Since they haven't, we can ignore them.
I shall ignore them when/if they are repeated and disproved. Until then I
provisionally believe in them, by which I mean I take the supplements.
Bayes' theorem and all that.
> If you want to try repeating them yourself and maybe be
> famous, be my guest.
If I were a multi-billionaire....
Cheers,
Michael C Price
Steve Harris
>> Actually, it doesn't (at least in mice): you should see the glucose
>> tolerance curves in my 40% CR animals-- horrible (abstract is below,
>> but it really takes looking at the graphs to get the full impact). Being
>> on severe CR doesn't give you a pancreas with a lot of reserve
>> (not surprisingly).
>> It's the average and fasting glucoses that are low in CR. 10% gives
>> intermediate fasting glucoses, and the best glucose tolerance to acute
>> challenge. Ad lib animals are pre-diabetic. Incidentally I did run
>> some of these on Cr picolinate for a while and got no glucose effect.
>
>Old, young or both?
Both as I recall.
>
>> I couldn't get ANY effect of this stuff in my model on ANY parameter.
>
>Including insulin levels?
I didn't look at that. My assay for insulin was not the most sensitive, and
I really couldn't reliably "see" any fasting insulin level differences even
among various fasting restriction groups. I saw a clear insulin signal only
with glucose challenge, and didn't look at glucose tolerance with chromium.
>You really should publish since it is impossible to critique unpublished
>word-of-mouth stuff.
Yep.
Chuck
Don't you mean calorie restriction?
Steve Harris
>> Mech Ageing Dev 1994 Mar;73(3):209-21 Related Articles, Books, LinkOut
>>
>>
>> Serum glucose, glucose tolerance, corticosterone and free fatty acids
during
>> aging in energy restricted mice.
>>
>> Harris SB, Gunion MW, Rosenthal MJ, Walford RL.
>>
>> Department of Pathology, University of California at Los Angeles 90024.
>>
>> Energy restriction, the only method known to increase maximum life span
in
>> laboratory animals
>
>Don't you mean calorie restriction?
Food energy's measured in calories (or actually, in the SI system, in
joules). Best to just say what you're really talking about. It's a "speed
limit" not a "miles per hour limit."
michaelprice
First, the RNA experiments demonstrating LE have been reproduced:
First done by Robertson, repeated by Gardner. Basic difference
was Gardner started on adult mice and lowered the dosage.
See:
The Effect of Yeast Nucleic Acid on the Survival Time of 600-Day-Old Albino
Mice by TS Gardner, Journal of Gerontology 3 (1946), pages 445-452.
Influence of Nucleic Acids of Various Origin upon the Growth and Longevity
of the white mouse by TB Robertson in the Australian J of Experimental
Biology and Medical Science, 5 pg 46-67, 1928
Second, the lower fasting glucose levels of Steve's CR "controls" is also
an effect produced by chromium picolinate, so they are not good controls.
Cheers,
Michael C Price
"michaelprice" <michae...@ntlworld.com> wrote in message
news:vkNn8.6$9t4....@news6-win.server.ntlworld.com...
Steve Harris
> Second, the lower fasting glucose levels of Steve's CR "controls" is also
> an effect produced by chromium picolinate, so they are not good controls.
How do you you figure? The CR animals got the same amount of brewer's yeast
per animal per day as the others.
Believe me, little bits of brewers yeast give or take make no difference in
this system. We tried giving non restricted and slightly restricted mice a
lot more of brewer's yeast; and we tried giving them a hellava lot of
straight red Cr-picolinate powder ("Chromax II"), as the pure chemical
provided from the nice people at Nutrition 21 in La Jolla, CA, 12.5%
chromium by weight (I'm sitting here, looking at the bottle as I type). And
we did both. There was no effect on glucose whatsoever. The restriction
effect on glucose is NOT a chromium effect. If it were, we've have swamped
it 3 ways from Sunday.
SBH
--
I welcome Email from strangers with the minimal cleverness to fix my address
(it's an open-book test). I strongly recommend recipients of unsolicited
bulk Email ad spam use "http://combat.uxn.com" to get the true corporate
name of the last ISP address on the viewsource header, then forward message
& headers to "abuse@[offendingISP]."
michaelprice
> "michaelprice" <michae...@ntlworld.com> wrote in message
> news:2uMp8.31201$gj7.4...@news2-win.server.ntlworld.com...
>
>> Second, the lower fasting glucose levels of Steve's CR "controls"
>> is also an effect produced by chromium picolinate, so they are
>> not good controls.
>
> How do you you figure? The CR animals got the same amount
> of brewer's yeast per animal per day as the others.
Sorry, you'll have to clue me in here. Brewer's yeast was used as
a source of B-vitamins or chromium GTF? Another thought, is the
strain you used susceptable to diabetes, like humans?
> Believe me, little bits of brewers yeast give or take make no
> difference in this system. We tried giving non restricted and
> slightly restricted mice a lot more of brewer's yeast; and we
> tried giving them a hellava lot of straight red Cr-picolinate powder
> ("Chromax II"), as the pure chemical provided from the nice people
> at Nutrition 21 in La Jolla, CA, 12.5% chromium by weight (I'm
> sitting here, looking at the bottle as I type). And we did both.
> There was no effect on glucose whatsoever. The restriction
> effect on glucose is NOT a chromium effect. If it were, we've
> have swamped it 3 ways from Sunday.
If you could measure no effect on any parameter with cr-pic, and
the animals are susceptable to diabetes, then this result seems at
odds with a number of human and other animal studies (e.g. pigs).
If they're not susceptable to diabetes then it might be a bad animal
model for humans.
For humans:
J Am Coll Nutr 1997 Oct;16(5):404-10 Related Articles, Books, LinkOut
Nutritional factors influencing the glucose/insulin system: chromium.
Anderson RA.
Nutrient Requirements and Functions Laboratory, United States Department of
Agriculture, Beltsville, Maryland 20705-2350, USA.
Chromium (Cr) improves the glucose/insulin system in subjects with
hypoglycemia, hyperglycemia, diabetes and hyperlipemia with no detectable
effects on control subjects. Chromium improves insulin binding, insulin
receptor number, insulin internalization, beta cell sensitivity and insulin
receptor enzymes with overall increases in insulin sensitivity. There have
been several studies involving Cr supplementation of subjects with NIDDM
and/or lipemia and most have reported beneficial effects of Cr on the
glucose/insulin system. In a recent study, Chinese subjects with NIDDM were
divided into three groups of 60 subjects and supplemented with placebo, 100
or 500 micrograms of Cr as chromium picolinate 2 times per day for 4 months.
Improvements in the glucose/insulin system were highly significant in the
subjects receiving 500 micrograms twice per day with less or no significant
improvements in the subjects receiving 100 micrograms twice per day after 2
and 4 months. In summary, Cr is involved in the control of the
glucose/insulin system and the amount, and likely form of chromium, are
critical when evaluating the role of chromium in this system.
Cheers,
Michael C Price
Steve Harris
> "Steve Harris" <sbha...@ix.RETICULATEDOBJECTcom.com> wrote in message
> news:a88je0$5i7$1...@slb4.atl.mindspring.net...
> > "michaelprice" <michae...@ntlworld.com> wrote in message
> > news:2uMp8.31201$gj7.4...@news2-win.server.ntlworld.com...
> >
> >> Second, the lower fasting glucose levels of Steve's CR "controls"
> >> is also an effect produced by chromium picolinate, so they are
> >> not good controls.
> >
> > How do you you figure? The CR animals got the same amount
> > of brewer's yeast per animal per day as the others.
>
> Sorry, you'll have to clue me in here. Brewer's yeast was used as
> a source of B-vitamins or chromium GTF?
Of GTF only. We had suspicions about the CrCl3 (as I remember) being used in
the AIN-76 mineral mix of the time. Or perhaps there was no Cr at all in
that mix-- I no longer remember. Anyhow restricted animals got about 60% of
the food of ad lib animals, so they were given a diet which was more dense
in vitamins, minerals and yeast by a factor of 1/0.6 = 5/3.
Another thought, is the
> strain you used susceptable to diabetes, like humans?
Not really. The ad libs ran glucoses around 120 mg/dL, which wouldn't
formally give them the diagnosis, even in todays' more conservative
atmosphere (where you need to be above 129). Perhaps a few were above 129,
but we'd have ignored them since the criteria then was 139. As a group, old
ad-lib fed C57Bl10/C3H hybrids are near diabetics, at best. For a real
diabetic, this control would be excellent with A1c's in the 6's.