Bruce Ames-ALA,,ALC results are in
Thomas Carter
Free full text will be available shortly after March 19. No word on
life span. I guess it will take several years to get such a study. The
LEF did some on ALA and ALC in '97, but I don't guess they combined
them as one treatment. Their studies on these substances and others
were obviously negative, since they won't publish results. IMO there
is a good chance this treatment will extend human, but not rodent
lives since they die of different diseases than we do. At any rate
some good curve squaring is not to be sneezed at either.
Thomas
Dietary supplements make old rats youthful, may help rejuvenate aging
humans, according to UC Berkeley study
Berkeley - Two dietary supplements straight off the health food store
shelf put the spark back into aging rats, and might do the same for
aging baby boomers, according to a study at the University of
California, Berkeley, and Children's Hospital Oakland Research
Institute.
A team of researchers led by Bruce N. Ames, professor of molecular and
cell biology at UC Berkeley, fed older rats two chemicals normally
found in the body's cells and available as dietary supplements:
acetyl-L-carnitine and an antioxidant, alpha-lipoic acid.
In three articles in the February 19 issue of Proceedings of the
National Academy of Sciences, Ames and his colleagues report the
surprising results. Not only did the older rats do better on memory
tests, they had more pep, and the energy-producing organelles in their
cells worked better.
"With the two supplements together, these old rats got up and did the
Macarena," said Ames, also a researcher at Children's Hospital Oakland
Research Institute (CHORI). "The brain looks better, they are full of
energy - everything we looked at looks more like a young animal."
"The animals seem to have much more vigor and are much more active
than animals not on this diet, signaling massive improvement to these
animals' health and well-being," said former UC Berkeley post-doctoral
fellow Tory M. Hagen, now an assistant professor at the Linus Pauling
Institute at Oregon State University, Corvallis. "And we also see a
reversal in loss of memory. That is a dual-track improvement that is
significant and unique. This is really starting to explode and move
out of the realm of basic research into people."
Based on the group's earlier studies, the University of California
patented use of the combination of the two supplements to rejuvenate
cells. Ames, through the Bruce and Giovanna Ames Foundation, and Hagen
founded a company in 1999 called Juvenon to license the patent from
the university. Juvenon currently is engaged in human clinical trials
of the combination.
One of the three PNAS articles probes the reasons behind this
rejuvenation, concluding that the two chemicals "tune up" the
energy-producing organelles that power all cells, the mitochondria.
Both chemicals are normally used in mitochondria.
Ames calls mitochondria the "weak link in aging." Evidence has been
piling up, he said, that deterioration of mitochondria is an important
cause of aging. A significant cause of this deterioration, he
believes, is the accumulation of destructive free radicals -
byproducts of normal metabolism - that disable enzymes and other
chemicals.
The combination therapy targets mitochondria to get rid of destructive
radicals and to boost the activity of a damaged enzyme, carnitine
acetyltransferase, that plays a key role in burning fuel in
mitochondria. The researchers hoped that the anti-oxidant alpha-lipoic
acid would do the former, and that flooding the cell with
acetyl-L-carnitine, one of two proteins that the enzyme acts on, would
achieve the latter.
Experiments showed that this regimen worked. Associate researcher
Jiankang Liu of CHORI, UC Berkeley postdoctoral fellow David W.
Killilea and Ames demonstrated that the enzyme carnitine
acetyltransferase is less active in old rats than in young rats, and
that it binds less tightly to acetyl-L-carnitine in older rats.
Supplementation with acetyl-L-carnitine or a combination of
acetyl-L-carnitine and alpha-lipoic acid restored the enzyme's
activity nearly to that found in young rats and substantially restored
binding to acetyl-L-carnitine.
"The acetyl-L-carnitine is protecting the protein and the higher
levels are enabling the protein to work, while alpha-lipoic acid
knocks down oxygen radicals," Ames said. "Each chemical solves a
different problem - the two together are better than either one
alone."
Ames and Hagen have long had an interest in mitochondria as they
relate to aging, and they were intrigued by a 1999 Italian study that
showed acetyl-L-carnitine, when fed to old rats, improved
mitochondrial activity.
The two thought this might be a way to reverse the effects of aging on
mitochondria, and in various trials found it to work to some degree.
Free radicals were still damaging the cell, however, so they decided
to pair it with one of the few antioxidants that gets into
mitochondria, alpha-lipoic acid. Lipoic acid is produced by
mitochondria and boosts levels of other antioxidants.
In the second of the PNAS studies, Hagen, Ames and colleagues compared
2- to 4-month-old rats to 24- to 28-month-old rats, all fed
acetyl-L-carnitine in their water and alpha-lipoic acid in their chow.
After as much as a month on the supplements, the old and lethargic
rats became more peppy, Ames said.
"We significantly reversed the decline in overall activity typical of
aged rats to what you see in a middle-aged to young adult rat 7 to 10
months of age," Hagen said. "This is equivalent to making a 75- to
80-year-old person act middle-aged. We've only shown short-term
effects, but the results give us the rationale for looking at these
things long term."
They found also that the combination of lipoic acid and
acetyl-carnitine improved mitochondrial activity and thus cellular
metabolism, and increased levels of various chemicals known to decline
with age, including ascorbic acid, an antioxidant.
In a third study, Liu, Hagen, Ames and colleagues fed old rats a
similar diet of the two supplements and looked at memory function as
measured by the Morris water maze test and a peak procedure for
assessing temporal or time-based memory developed by Seth Roberts,
professor of psychology at UC Berkeley. They found that
supplementation improved both spatial and temporal memory, and reduced
the amount of oxidative damage to RNA in the brain's hippocampus, an
area important in memory. In electron microscope pictures of cells
from the hippocampus, mitochondria showed less structural decay in old
rats that had a supplemented diet.
"We did two different tests for cognitive activity in rats, and in
both it made a big difference to feed them this mixture," Ames said.
"Memory degenerates with age, and this makes them better."
The analysis of nucleic acid damage in the brain was performed with
post-doctoral researcher Elizabeth Head and Carl W. Cotman, professor
of neurobiology and behavior, at the Institute for Brain Aging and
Dementia at UC Irvine. UC Berkeley psychology graduate student Afshin
M. Gharib worked with Liu to conduct the peak performance tests.
"In aging, you're oxidizing the proteins in mitochondria and they lose
activity," Ames explained. "If some of that lost activity is due to
binding for substrate or coenzyme - like binding of acetyl-L-carnitine
by carnitine acetyltransferase - and you can raise the level of those,
then you can reverse some of the loss.
"We showed, in fact, that that is what's happening with
acetyl-L-carnitine. Aldehydes from lipid oxidation are glomming onto
that protein, and that is what appears to cause the reduction in
binding activity. But if you raise the level of acetyl-L-carnitine,
now it works."
Hagen added, "With aging, we see so many different things that are
occurring to mitochondria that then lead to consequences in the cell.
If you tune up mitochondria you may have a means of at least delaying
the onset of a number of age-related problems that we encounter, or we
can in some ways, hopefully, reverse what has already taken place."
michaelprice
Any news on the amounts the rats received?
Cheers,
Michael C Price
"Thomas Carter" <tcar...@elp.rr.com> wrote in message
news:a7b55247.02021...@posting.google.com...
Tim
Tim
Tim
http://patft.uspto.gov/netahtml/search-bool.html
Type in 6335361
Arto Raiskio
http://patft.uspto.gov/netacgi/nph-Parser?Sect2=PTO1&Sect2=HITOFF&p=1&u=%2Fn
etahtml%2Fsearch-bool.html&r=1&f=G&l=50&d=PALL&RefSrch=yes&Query=PN%2F591691
2
--
.
"Tim" <timo...@my-deja.com> wrote in message
news:6da4c14.02021...@posting.google.com...
Randall Parker
http://www.sciencedaily.com/releases/2002/02/020219075823.htm
I'm very curious to see what Aubrey has to say about these results.
stu
combination (lipoic acid & l-carnitine) in their Chronoforte product
for ages?
Aubrey de Grey
Randall Parker wrote:
> I'm very curious to see what Aubrey has to say about these results.
Yeah, it's been a busy journalistic day for a lot of us. In short, I'm
a little surprised that this work has received as much media attention
as it has, because it's only a rather minor extension of work from Ames
and Hagen published over the past few years. Specifically, they show
increases in mitochondrial function and its natural consequences (like
activity) and they figure out a few things about its molecular etiology,
but they still have no lifespan data. I remain cautious that an effect
on lifespan will be found, because I suspect that the age-related loss
of mitochondrial activity is an adaptive response to other things --
things which are not being fixed by this treatment -- and thus that the
restoration of that activity, while beneficial in the short term, may
be ineffective or even harmful in the longer term. This is particularly
so in view of the fact that both the compounds being supplemented are
ones that cells already make. It's rather the same deal as with growth
hormone: short-term benefits but substantial side-effects.
Aubrey de Grey
Max Watt
> again no mention of use of r-enantiomer or s-enantiomer lipoic acid ?
>
> http://patft.uspto.gov/netacgi/nph-Parser?Sect2=PTO1&Sect2=HITOFF&p=1&u=%2Fn
> etahtml%2Fsearch-bool.html&r=1&f=G&l=50&d=PALL&RefSrch=yes&Query=PN%2F591691
> 2
I was R-lipoic acid in their studies. The patent was cast to be
voerly broad to prevent others from using slight variants. It also
stated other antioxidants could be used without specifying them, so as
ot cover anyone's possible future improvements.
Tim
Tim
stu
here. Or do you think there may be downsides to the Lipoic acid as
well?
Stu
ag...@mole.bio.cam.ac.uk (Aubrey de Grey) wrote in message news:<a4udne$nsp$1...@pegasus.csx.cam.ac.uk>...
Te...@aor.ca
> Hi,
> Free full text will be available shortly after March 19. No word on
> life span. I guess it will take several years to get such a study. The
> LEF did some on ALA and ALC in '97, but I don't guess they combined
> them as one treatment. Their studies on these substances and others
> were obviously negative, since they won't publish results.
The reason for this failure might very well be the fact that the Life
Extension Foundation studies used the racemate. A published study from
Germany found that R(+)-lipoic aci, but not the racemate, extended life
in NMRI mice.
The scientists fed their animals either a basic lab animal diet, or one
supplemented with equal doses (75 milligrams per kilogram of body weight)
of one of the three forms of lipoic acid, starting the experiment when the
animals were ten weeks old and continuing on for the rest of their lives.
The time it took for half of the animals in each group to die was not
changed by any form of lipoic acid, suggesting that none of the
supplements had any effect on simple things like short-term vulnerability
to an infection or parasites. But among the animals who made it past the
halfway point, a dramatic difference emerged.
Animals whose diets were supplemented with the racemic compound lived no
longer than they would have if they had eaten the basic, unsupplemented
diet. If anything, their lives were slightly shorter, although the
difference was not strong enough to rule out a simple statistical fluke:
the maximum lifespan among the animals who ate the unsupplemented lab food
was 26 weeks from the beginning of the study, but the longest-lived animal
receiving the racemic compound died at 23 weeks.
Similarly, the animals who got the S(-)-enantiomer seemed to live a little
longer than the unsupplemented animals (one animal survived 29 weeks from
the introduction of the artificial enantiomer into its diet) – but, again,
the difference was not large enough to be a statistically meaningful
result.
In short, neither the racemate form of lipoic acid you get in common
supplements, nor straight S(-)-lipoic acid, seems to have done anything
notable to these animals, for better or for worse. They may as well have
been eating regular lab chow.
But the results in the animals who were given access to a diet enriched
in R(+)-Lipoic Acid were undeniable. The longest-lived animals in this
group lived dramatically longer lives than those in any other cohort. Long
after all of the animals getting unsupplemented rat chow, or the synthetic
S(-)-lipoic acid, or the racemic compound were dead, animals whose diets
were supplemented with R(+)-Lipoic Acid were still alive. The last one
gave up the ghost fully 38 weeks after the beginning of the experimental
diets.
Freisleben HJ, Neeb A, Lehr F, Ackermann H. Influence of selegiline or
lipoic acid on the life expectancy of immunosuppressed mice.
Arzneimittelforschung. 1997 Jun;47(6):776-80.
Dr. Hagen's and Dr. Ames' dramatic new results were obtained using
R(+)-lipoic acid.
Proc. Natl. Acad. Sci. USA, Vol. 99, Issue 4, 2356-2361, February 19, 2002
Memory loss in old rats is associated with brain mitochondrial decay and
RNA/DNA oxidation: Partial reversal by feeding acetyl-L-carnitine and/or
R-alpha-lipoic acid
Jiankang Liu, Elizabeth Head, Afshin M. Gharib, Wenjun Yuan, Russell T.
Ingersoll, Tory M. Hagen, Carl W. Cotman, and Bruce N. Ames.
Accumulation of oxidative damage to mitochondria, protein, and nucleic
acid in the brain may lead to neuronal and cognitive dysfunction. The
effects on cognitive function, brain mitochondrial structure, and
biomarkers of oxidative damage were studied after feeding old rats two
itochondrial metabolites, acetyl-L-carnitine (ALCAR) [0.5% or 0.2%
(wt/vol) in drinking water], and/or R-alpha-lipoic acid (LA) [0.2% or 0.1%
(wt/wt) in diet]. Spatial memory was assessed by using the Morris water
maze; temporal memory was tested by using the peak procedure (a time-
discrimination procedure). Dietary supplementation with ALCAR and/or LA
improved memory, the combination being the most effective for two
different tests of spatial memory (P < 0.05;
P < 0.01) and for temporal memory (P < 0.05). Immunohistochemical analysis
showed that oxidative damage to nucleic acids (8-hydroxyguanosine and
8-hydroxy-2'-deoxyguanosine) increased with age in the hippocampus, a
region important for memory. Oxidative damage to nucleic acids occurred
predominantly in RNA. Dietaryadministration of ALCAR and/or LA
significantly reduced the extent of oxidized RNA, the combination being
the most effective.
Electron microscopic studies in the hippocampus showed that ALCAR and/or
LA reversed age-associated mitochondrial structural decay. These results
suggest that feeding ALCAR and LA to old rats improves performance on
memory tasks by lowering oxidative damage and improving mitochondrial
function.
___________________________________________________________________________
Proc. Natl. Acad. Sci. USA, Vol. 99, Issue 4, 1870-1875, February 19, 2002
Feeding acetyl-L-carnitine and lipoic acid to old rats significantly
improves metabolic function while decreasing oxidative stress.
Tory M. Hagen, Jiankang Liu, Jens Lykkesfeldt, Carol M. Wehr, Russell T.
Ingersoll, Vladimir Vinarsky, James C. Bartholomew, and Bruce N. Ames.
Mitochondrial-supported bioenergetics decline and oxidative stress
increases during aging. To address whether the dietary addition of
acetyl-L-carnitine [ALCAR, 1.5% (wt/vol) in the drinking water] and/or
(R)-alpha-lipoic acid [LA, 0.5% (wt/wt) in the chow] improved these
endpoints, young (2-4 mo) and old (24-28 mo) F344 rats were supplemented
for up to 1 mo before death and hepatocyte isolation. ALCAR+LA partially
reversed the age-related decline in average
mitochondrial membrane potential and significantly increased (P = 0.02)
hepatocellular O2 consumption, indicating that mitochondrial-supported
cellular metabolism was markedly improved by this feeding regimen.
ALCAR+LA also increased ambulatory activity in both young and old rats;
moreover, the improvement was significantly greater (P = 0.03) in old
versus young animals and
also greater when compared with old rats fed ALCAR or LA alone. To
determine whether ALCAR+LA also affected indices of oxidative stress,
ascorbic acid and markers of lipid peroxidation (malondialdehyde) were
monitored. The hepatocellular ascorbate level markedly declined with age
(P = 0.003) but was restored to the level seen in young rats when ALCAR+LA
was given. The level of malondialdehyde, which was significantly higher (P
= 0.0001) in
old versus young rats, also declined after ALCAR+LA supplementation and
was not significantly different from that of young unsupplemented rats.
Feeding ALCAR in combination with LA increased metabolism and lowered
oxidative stress more than either compound alone.
___________________________________________________________________________
Proc. Natl. Acad. Sci. USA, Vol. 99, Issue 4, 1876-1881, February 19, 2002
Age-associated mitochondrial oxidative decay: Improvement of carnitine
acetyltransferase substrate-binding affinity and activity in brain by
feeding old rats acetyl-L-carnitine and/or R-alpha-lipoic acid.
Jiankang Liu, David W. Killilea, and Bruce N. Ames.
We test whether the dysfunction with age of carnitine acetyltransferase
(CAT), a key mitochondrial enzyme for fuelutilization, is due to decreased
binding affinity for substrate and whether this substrate, fed to old
rats, restores CAT activity. The kinetics of CAT were analyzed by using
the brains of young and old rats and of old rats supplemented for 7 weeks
with the CAT substrate acetyl-L-carnitine (ALCAR) and/or the mitochondrial
antioxidant precursor R-alpha-lipoic acid (LA). Old rats, compared with
young rats, showed a decrease in CAT activity and in CAT-binding affinity
for both substrates, ALCAR and CoA. Feeding ALCAR or ALCAR plus LA to old
rats significantly restored CAT-binding affinity for ALCAR and CoA, and
CAT activity. To explore the underlying mechanism, lipid peroxidation and
total iron and copper levels were assayed; all increased in old rats.
Feeding old rats LA or LA plus ALCAR inhibited lipid peroxidation
but did not decrease iron and copper levels. Ex vivo oxidation of
young-rat brain with Fe(II) caused loss of CAT activity and binding
affinity. In vitro oxidation of purified CAT with Fe(II)
inactivated the enzyme but did not alter binding affinity. However, in
vitro treatment of CAT with the lipid peroxidation products
malondialdehyde or 4-hydroxy-nonenal caused a decrease
in CAT-binding affinity and activity, thus mimicking age-related change.
Preincubation of CAT with ALCAR or CoA prevented malondialdehyde-induced
dysfunction. Thus, feeding old rats high
levels of key mitochondrial metabolites can ameliorate oxidative damage,
enzyme activity, substrate-binding affinity, and mitochondrial
dysfunction.
___________________________________________________________________________
Our first lot of R(+)-lipoic acid is now sold out. However, a second batch
should be available in Canada within two weeks. AOR's R(+)-lipoic acid
will be distributed in America through Jarrow Formulas, and may also be
made available through a second, mail-order distributor.
To your health!
AOR
--
ADVANCED ORTHOMOLECULAR RESEARCH is Canada's most advanced supplement
line. AOR was the first to make SAMe, Pantethine, anti-aging Carnosine,
and Prostaphil defined pollen extract, available to Canadians.
http://www.holisticinternational.com http://www.R-Lipoic.com
Thomas Carter
> Thomas Carter wrote:
>
> > Hi,
> > Free full text will be available shortly after March 19. No word on
> > life span. I guess it will take several years to get such a study. The
> > LEF did some on ALA and ALC in '97, but I don't guess they combined
> > them as one treatment. Their studies on these substances and others
> > were obviously negative, since they won't publish results.
>
> The reason for this failure might very well be the fact that the Life
> Extension Foundation studies used the racemate.
Yes, could be, or it could be that they did't combine the treatments,
or that they tested for life span which Ames, Hagen did not.
> A published study from
> Germany found that R(+)-lipoic aci, but not the racemate, extended life
> in NMRI mice.
> The scientists fed their animals either a basic lab animal diet, or one
> supplemented with equal doses (75 milligrams per kilogram of body weight)
> of one of the three forms of lipoic acid, starting the experiment when the
> animals were ten weeks old and continuing on for the rest of their lives.
> The time it took for half of the animals in each group to die was not
> changed by any form of lipoic acid, suggesting that none of the
> supplements had any effect on simple things like short-term vulnerability
> to an infection or parasites. But among the animals who made it past the
> halfway point, a dramatic difference emerged.
>
> Animals whose diets were supplemented with the racemic compound lived no
> longer than they would have if they had eaten the basic, unsupplemented
> diet. If anything, their lives were slightly shorter, although the
> difference was not strong enough to rule out a simple statistical fluke:
> the maximum lifespan among the animals who ate the unsupplemented lab food
> was 26 weeks from the beginning of the study, but the longest-lived animal
> receiving the racemic compound died at 23 weeks.
>
> Similarly, the animals who got the S(-)-enantiomer seemed to live a little
> longer than the unsupplemented animals (one animal survived 29 weeks from
> the introduction of the artificial enantiomer into its diet) – but, again,
> the difference was not large enough to be a statistically meaningful
> result.
>
> In short, neither the racemate form of lipoic acid you get in common
> supplements, nor straight S(-)-lipoic acid, seems to have done anything
> notable to these animals, for better or for worse. They may as well have
> been eating regular lab chow.
>
> But the results in the animals who were given access to a diet enriched
> in R(+)-Lipoic Acid were undeniable.
The abstract says not significant
> The longest-lived animals in this
> group lived dramatically longer lives than those in any other cohort. Long
> after all of the animals getting unsupplemented rat chow, or the synthetic
> S(-)-lipoic acid, or the racemic compound were dead, animals whose diets
> were supplemented with R(+)-Lipoic Acid were still alive. The last one
> gave up the ghost fully 38 weeks after the beginning of the experimental
> diets.
>
> Freisleben HJ, Neeb A, Lehr F, Ackermann H. Influence of selegiline or
> lipoic acid on the life expectancy of immunosuppressed mice.
> Arzneimittelforschung. 1997 Jun;47(6):776-80.
Here's the abstract.
Arzneimittelforschung 1997 Jun;47(6):776-80
Influence of selegiline and lipoic acid on the life expectancy of
immunosuppressed mice.
Freisleben HJ, Neeb A, Lehr F, Ackermann H.
Gustav-Embden-Zentrum der Biologischen Chemie, Laboratorium fur
Mikrobiologische
Chemie, Frankfurt/Main Germany.
Ten groups of 14 immunosuppressed NMRI-mice (nu/nu) were raised and
kept under
germ-reduced conditions. The control animals were fed a germ-reduced
diet, nine
other groups received the same diet with selegiline (CAS 14611-51-9,
Deprenyl)
or lipoic acid (thioctic acid, CAS 62-46-4) admixed at various
amounts. The 50%
survival rate, the total life span of each group and the areas under
the curves
were determined to evaluate life expectancy as compared to the
controls. The
racemate of lipoic acid at high dosage (350 mg/kg body weight) reduced
the life
span significantly. The S(-)-enantiomer of lipoic acid (75 mg/kg body
weight)
increased the 50% survival rate, whereas the physiologic
R(+)-enantiomer (9
mg/kg body weight) expanded the total life span of its group.
Alteration of only
one out of three parameters was not considered significant. All other
groups
except for one did not differ from controls: only animals which
obtained 75
micrograms selegiline per kg of body weight and per day exerted
increased life
expectancies by all three parameters. This group exhibited also in
statistical
evaluation a significantly (p < 0.05) prolongated survival time up to
about 200%
as compared to the control animals.
PMID: 9239459
The abstract doesn't bear out your claims. If you have a copy of the
full text, and will send it to me, I will verify your claims for the
newsgroup.
This is the second time you've posted here with spurious claims
desinged to sell your product. Never the less the evidence for the R
form now seems to be quite a bit stronger than when we discussed it
before. I seem to remember some non peer reviewed claims in Packer's
Patent brief which now seem possibly more plausable. Some thing like
seven times more mitochondrial absorption. IIRC.
I would guess it will take something like three years minimum
before we can get reliable info on the differences between these two
substances. I am strongly considering a switch at least in part to the
R form until more info is in.
Thx for the info.
Thomas
snip>
Aubrey de Grey
Stu wrote:
> Aubrey, I guess you are referring to the Acetyl-L-Carnitine component
> here. Or do you think there may be downsides to the Lipoic acid as
> well?
I'm much less sure about lipoic acid. The argument that we probably
make the ideal amount of it still applies, but (a) that's in a context
of normal ALCAR concentrations -- it's reasonable that the body might
not know what to do about weirdly high concentrations -- and (b) there
is nothing obviously wrong with having lots of ALA, so one has to fall
back on the generalisation that antioxidants become pro-oxidant at
excessive concentrations.
Aubrey de Grey
Tom Matthews
> Stu wrote:
>
>
>>Aubrey, I guess you are referring to the Acetyl-L-Carnitine component
>>here. Or do you think there may be downsides to the Lipoic acid as
>>well?
>>
>
> I'm much less sure about lipoic acid. The argument that we probably
> make the ideal amount of it still applies,
That is a purely evolutionary argument which I think is rather weak when
you try to apply it across the board to all biochemical processes for a
species such as homo sapiens which has been changing in environment and
general lifestyle at an enormous rate compared with what evolution can
reasonably achieve.
> but (a) that's in a context
> of normal ALCAR concentrations -- it's reasonable that the body might
> not know what to do about weirdly high concentrations --
I must reject this use of the word "weird". Yes, a natural human body
has not seen those concentrations before, but so what? If we are ever to
achieve a major lengthening of our lifespan then we certainly *must* to
"weird" things of one kind or another to our bodes!
> and (b) there
> is nothing obviously wrong with having lots of ALA, so one has to fall
> back on the generalisation that antioxidants become pro-oxidant at
> excessive concentrations.
I think the operative word here is "excessive". IMO, this may vary
greatly depending on the cell and tissue type, and the disease state,
including age.
--Tom Matthews
MoreLife for us all - http://morelife.org
Reality based tools for More Life in quantity & quality
stu
become pro-oxidant? If we take large quantities of ALA should we boost
specific compounds to compensate?
Stu
Tom Matthews <t...@morelife.org> wrote in message news:<3C7A86C5...@morelife.org>...
DB
The ALA quenches itself.
DB
Te...@aor.ca
Te...@AOR.ca wrote in message news:<3C742005...@AOR.ca>...
> Thomas Carter wrote:
>
> > Hi,
> > Free full text will be available shortly after March 19. No word on
> > life span. I guess it will take several years to get such a study. The
> > LEF did some on ALA and ALC in '97, but I don't guess they combined
> > them as one treatment. Their studies on these substances and others
> > were obviously negative, since they won't publish results.
>
> The reason for this failure might very well be the fact that the Life
> Extension Foundation studies used the racemate.Yes, could be, or it could be that they did't combine the treatments,
or that they tested for life span which Ames, Hagen did not.
Dr. Ames and Dr. Hagen are doing lifespan studies now. In October of 2000, Dr. Ames stated in the Sens - Transcript that "We've had trouble getting the lipoic acid from this company in Germany, and we had trouble getting the rats from NIA, and there've been various pitfalls, but it's
> A published study from
> Germany found that R(+)-lipoic aci, but not the racemate, extended life
> in NMRI mice.
The abstract says not significant
That is reasonable. Please send me your address or fax number and I will send you a copy to confirm these statements.
Tom Matthews
> Thomas Carter wrote:
>
> The abstract doesn't bear out your claims. If you have a copy of the
> full text, and will send it to me, I will verify your claims for the
> newsgroup.
>
> That is reasonable. Please send me your address or fax number and I will
> send you a copy to confirm these statements.
Would you please Fax me a copy also. 559-663-5511
Dave
Dave
Tom Matthews wrote:
--
The following is my e-mail address in ASCII numerical form:
100 97 106 64 110 101 116 49 112 108 117 115 46 99 111 109
To e-mail me, covert back to corresponding characters.
To the best of my knowledge the address harvesters have
not yet caught on to this method. :-)