List, I know that this has come up before, but I stress that yall must
at least give this a try. Thanks to Dens suggestion on the l-carnitine,
my father is much better, the results were seen in only 5 days! I have
been researching for weeks now for any side effects to this supplement,
prior to giving this to my son, the only thing that I have been able to
uncover is slight diarrhea when the dosage is extremely high. There are
no long term effects, and l-carnitine is used in hospitals with patients
with heart failure with excellent results. L-carnitine can be purchased
over-the-counter, and we got ours from GNC, the liquid form.
                            Best Wishes Linda Forrest's Mom

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THERAPIES TO SLOW BRAIN AGING
When our brain ages, our body follows. The brain controls all our life
systems. Its 10 billion neurons and supporting glial cells define our
identity and generate our thoughts and feelings. When our brain cells
malfunction or die, our memories fade, our thinking ability disappears,
our muscles atrophy, our bones become brittle, our arteries harden, our
immune system weakens, our coordination declines, and our life begins to
slip away.
In seeking to derail aging, there's nothing more important than our
brain. Therapies that slow brain aging pay multiple dividends; they help
to maintain our identity, while preserving the vital functions that
enable us to enjoy our lives in good health and vigor. There is
considerable evidence that a wide variety of compounds have beneficial
effects on brain aging, including vitamin E, selenium, beta-carotene,
hydergine, piracetam, centrophenoxine, phosphatidylcholine, and
phosphatidylserine. Based upon current evidence however, the two most
potent anti-aging therapies for the brain are DEPRENYL and
ACETYL-L-CARNITINE.


ALC AND BRAIN AGING

Researchers have shown that age-dependent brain cell changes can be
slowed or prevented by treatment with Acetyl-l-carnitine (ALC). In one
study at the University of Tor Vergata in Rome (Arch Gerontol Geriatr,
10:173-185:1 990), scientists used ALC to prevent the age-dependent loss
of neurons in certain areas of the rat brain, especially the
hippocampus, one of the primary memory centers in the brain.
The benefits of ALC's ability to protect neurons in the memory center of
rats can be seen in a study in which treatment for eight months with ALC
prevented the age-related loss of the ability of rats to find their way
through a radial maze (Prog Neuro Psychopharmacol & Biol Psychiat, 1 4
:359-369 :1 990).


NERVE GROWTH FACTOR MAINTAINS YOUTHFUL NEURONS

There is solid evidence that many of the neurodegenerative changes
associated with brain aging may be caused, in part, by a decline in the
activity of a class of neurochemicals called Nerve Growth Factor (NGF)
that provide support for the healthy functioning of brain cells,
especially in the hippocampus and frontal cortex of the brain.
(Molecular Brain Research, 3:55-60:1987). Further evidence that the
decline in NGF is a cause of the degeneration of brain cells comes from
studies in which intracere broventricular infusion of NGF was able to
reverse both structural and behavioral deficits in aged rats. (Nature,
329:6568:1 987).

ALC BOOSTS NGF LEVELS

A recent study at the University of Rome in Italy provides striking new
evidence to explain the anti-aging benefits of Acetyl-l-carnitine in
improving cognitive and behavioral function in aging humans
(Experimental Gerontology, 29:55-66:1994). In this study, ALC was
dissolved in the drinking water of rats (at a dosage level of 150mg/kg
per day) for six months, starting at the advanced age of 21 months. In
another part of the study, ALC was injected intraperitoneally (100mg\kg)
twice a day for eight consecutive days.
The scientists found that both short term and long-term administration
of ALC increased NGF levels by 39% in the central nervous system (CNS)
of aging rats. Moreover,long-term treatment with ALC completely
prevented the loss of choline acetyltransferase (CHAT) activity in the
brain of these rats. CHAT is the enzyme that helps to transform the
nutrient choline into the neurotransmitter acetylcholine, which plays an
essential role in learning and memory.

The scientists concluded that: "These results indicate that short term
treatment with ALC is able to induce NGF production and its subsequent
utilization in the CNS of aged rats, whereas treatment with ALC which
starts at a time when senescence-related CNS impairments are taking
place will protect neurons by maintaining NGF activity. This would imply
for ALC either curative properties when given to aged subjects, or
preventive properties when administered to aging ones".


AN EFFECTIVE ANTI-AGING TREATMENT IN HUMANS

These findings help to explain how ALC can slow down the deterioration
of Alzheimer's patients. In one such study at the Institute Mario Negri
in Milan, Italy, 130 patients with Alzheimer's Disease were given 2
grams a day of ALC for a year and were compared to patients receiving
placebo (Neurology, 41:17261732 1991). The results showed a markedly
slower rate of deterioration in patients receiving acetyl-l-carnitine in
13 of the 14 functions measured!
They also suggest that ALC might be even more beneficial in slowing or
preventing cognitive and behavioral deficits in normally-aging persons
without overt signs of disease. The evidence suggests that, at a
minimum, long-term treatment with Acetyl-l-carnitine could stop us from
getting age related neurodegenerative diseases such as Alzheimer's
Disease and, at best, could slow normal aging in humans dramatically.
1.Arch Gerontol Geriatr, 10:173-185:1990
2.Prog Neuro-Psychopharacol & Biol Psychiat, 14:359-369:1990
3.Molecular Brain Research, 3:55-66:1987
4.Nature, 329:65-68:1987
5.Experimental Gerontology, 29:55-66:1994
6.Neurology, 41:1726-1732:1991

ACETYL L-CARNITINE AND L-CARNITINE BOOSTS DNA REPAIR

New research offers strong evidence that L-Carnitine and
Acetyl-l-Carnitine can greatly effect the repair of DNA damage in
peripheral blood Iymphocytes (white blood cells), suggesting that both
compounds can help to prevent the age-related decline of the immune
system and, perhaps, other systems as well. DNA repair is at the very
heart of all our life functions and any therapy that can aid this
process is of great value.
The DNA in the nucleus of our cells contains the blueprint for the
healthy functioning of the entire organism. If the double-stranded DNA
molecule-which includes the chromosomes that harbor the genes that
control our every function-fails to maintain its structural integrity,
the results can be catastrophic cell death, soon resulting in the death
of the organism.

Our DNA is constantly subject to attack from radiation and chemicals in
our food, water, and air. These attacks cause frequent structural and
sequential damage to one or both DNA strands, which would lead rapidly
to massive cell death if it wasn't for nuclear enzymes that constantly
repair DNA damage. One of the most studied method of DNA repair is the
"cut-and-patch" method in which the damaged components of DNA
(nucleotides) are excised by "cutting" enzymes followed by the synthesis
of healthy replacem ent nucleotides in the appropriate order.

DNA repair is an absolutely critical function - it maintains the healthy
function of our cells and may play a critical role in the rate of normal
aging and the determination of maximum lifespan in different species.
It's also been suggested that diminished DNA repair capacity may play an
important role in our progressively higher risk of Alzheimer's disease,
Parkinson's disease, and other neurodegenerative diseases with
increasing age.

There are several well-documented DNA repair disorders, including
Xeroderma Pigmentosum (XP), Cockayne's Syndrome (CS), and Fanconi's
Anemia (FA) that are characterized by increased sensitivity to the
cell-destroying effects of ultra-violet radiation or agents that cause
DNA interstrand cross-linking. Recently, the genes responsible for
defective DNA repair in Xeroderma Pigmentosum, Cockayne's Syndrome , and
Fanconi's Anemia have been cloned and characterized.

In addition to the above diseases in which defective DNA repair has been
established as a causal factor, it's also been proposed that an altered
response to DNA damage may, in part, be responsible for the development
of a variety of of neurodegenerative diseases including Alzheimer's
disease. Indeed, there is evidence that Peripheral Blood Lymphocytes
(PBLs) sampled from patients with Alzheimer's disease are especially
defective in the removal of single-strand DNA breaks.

A recent study conducted by scientists from the U.S., Italy, and The
Netherlands sought to determine whether the addition of varying doses of
L-Carnitine and Acetyl-L-Carnitine to cultured Peripheral Blood
Lymphocytes exposed to several DNA-damaging agents could improve DNA
repair in these cells4.

The study utilized several oxygen-radical generating agents (Xanthine
Oxidase (XOD), Hypoxanthine (HYP), and the alkylating agent ENU) to
mimic the conditions of DNA strand damage caused by reperfusion
following ischemia (loss of oxygenated blood flow). . They discovered
that these agents induced a large number of single-strand DNA breaks
(SSB) in cultured peripheral blood lymphocytes. They then treated the
damaged DNA strands with either L-Carnitine or Acetyl-L-Carnitine.

The researchers found that treatment with either L-Carnitine or
Acetyl-L-Carnitine caused the disappearance of the vast majority of the
single-strand breaks that had been induced in the cells. As they put it
" . . . at 24 hours after treatment the elution curves of treated cells
were practically indistinguishable from elution curves of control cells,
indicating complete repair of the induced SSBs."

The scientists concluded that: "The ability to remove DNA lesions at an
increased rate should be of great importance in maintaining correct
cellular functioning and in ensuring survival. In particular, those DNA
damages that appear to be removed at a slow rate, or seem to persist in
the genome may gradually accumulate in target genes and result in the
slow deterioration of essential gene functioning until cell death
occurs."

L-Carnitine has been shown to protect heart tissue against ischemia, to
improve cardiac performance, and to restore high-energy phosphate pools
that contribute to the generation of energy molecules (ATP) in heart
cells. Acetyl-l-Carnitine has been shown to increase energy within
neurons, to improve learning and cognitive abilities, and to improve the
condition of patients suffering from neurodegenerative diseases such as
Alzheimer's disease.

Recently, Kalaria and Harik reported a 25%-to-40% decrease in t he
mitochondrial enzyme (carnitine acetyl-transferease) that plays a key
role in energy production within brain cells in both the frontal and
temporal cortex of patients with Alzheimer's disease5. This enzymatic
decrease may explain the benefits for such patients of taking
Acetyl-l-Carnitine, as well as its benefits for normally aging persons.

1.Nucleic Acids Res, 19:6301-6308, 1991 - Nature, 356:763-767, 1992
2.J Gerontol Biol Sci, 47:B177 -B184, 1992 - J Amer Geriatr Soc,
35:532-541, 1987
3.Neurobiol Aging, 12:367370, 1991
4.Carcinogenesis, 14:10:L2131-2136, 1993
5.Am Neurol, 32:583-586, 1992
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