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
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
"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
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,
"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-L-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."
Source: University Of California - Berkeley 2002
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