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ANTI-AGING
DRUGS AND SUPPLEMENTS |
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5.1
DRUGS THAT ARE HIGHLY RECOMMENDED (for inclusion in
your supplementation anti-aging program) |
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In the early 1960's
Professor Joseph Knoll of Semmelweis University in
Hungary developed the medication Deprenyl for use
as an anti-depressant. Later the drug was found to
benefit Parkinson's patients due to it's ability to
regulate neurotransmitters such as dopamine. Parkinson's
is thought to be caused by low-production of dopamine.
Dopamine production in such patients decreases by
30% to 90% per decade, and when production has fallen
to 10% of normal the patient dies within a short time.
Dopamine production also decreases in healthy people,
but at a slower rate of about 13% per decade in normally
aging people and only 8% in slowly aging people. However,
the difference in Parkinson's patients and healthy
people is only a matter of rate of decline and time.
A study done in 1988 by Professor Knoll showed that
rats given medium does of Deprenyl live up to
thirty percent longer because the drug slows this
loss of dopamine. Later experiments also showed
increased life-span, although not as high a percent
as the 1988 experiment found.
Originally, the
drug was thought to work only as an MAO-inhibitor
(MAO, or monoamine oxidase, is the neurotransmitter
that metabolizes used neurotransmitters). When MAO-levels
rise, as they do as a person ages, levels of neurotransmitters
such as dopamine, decrease. MAO-inhibitors help stabilize
levels of neurotransmitters and thus slow aging. However,
research from 1994 shows Deprenyl has benefits unconnected
with its MAO-inhibiting action. Deprenyl also
acts as an anti-oxidant and stimulates production
of the body's natural anti-oxidant enzymes superoxide
dismutase (SOD) and catalase (CAT). These effects
also slow aging.
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Professor
Joseph Knoll, discover of the pharmacological
activity of Deprenyl |
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Parkinson's disease
is currently the only FDA approved use of the drug,
but there is on-going research on its use to treat
Alzheimer's. Anecdotal evidence indicates that Deprenyl
may be effective in treating stoke, dementia, multiple
scelrosis, and hypertension, and a number of other
conditions. Dr. Clyde Reynolds, a specialist in metabolic
cancer therapy in Washington State, discovered that
cancer patients consistently have imbalances in the
neurotransmitters epinephrine, norepinephrine, and
serotonin and the balance must be restored if patients
are to be cured. This is possibly due to Deprenyls
ability to increase DHEA levels, which are
important in maintaining the immune system.
Another benefit of Deprenyl
is its aphrodisiac effect and its ability to increase
sensitivity of touch. Research done by Professor
Knoll in 1993 found increased mating frequency in
rats and incidental evidence from those people taking
Deprenyl concurs.
Healthy individuals looking
at Deprenyl for life-extension purposes are advised
moderate doses. Over the long term, proper dosage
appears to be a crucial factor and research is underway
to pin-point optimum dosage. Very high doses are not
advised for healthy people. The following rate is
currently recommended for starting dosage and should
be lowered after several months of treatment:
| Age |
Dosage |
Age |
Dosage |
| 30-35 |
1mg
twice a week |
60-65 |
5
mg every day |
| 35-40 |
1mg
every other day |
65-70 |
6mg
every day |
| 40-45 |
1mg
every day |
70-75 |
8mg
every day |
| 45-50 |
2mg
every day |
75-80 |
9mg
every day |
| 55-60 |
3mg
every day |
80
and over |
10mg
every day |
Selected references on Deprenyl:
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Department of Pharmacology, Semmelweis
University of Medicine, Budapest, Hungary.
Long-term experiments on male
rats revealed that better performers in the mating test
are better learners in the shuttle box and the more
active animals live significantly longer than their
less active peers. It was established by the aid of
(-)Deprenyl, a highly specific chemical tool, which
increases superoxide dismutase activity in the striatum,
facilitates the activity of the nigrostriatal dopaminergic
neurons with utmost selectivity, and protects these
neurons from their age-related decay, that the efficiency
of a male rat in behavioral tests, as well as the duration
of its life are striatal dopamine dependent functions.
As a measure of striatal function, sexual activity was
tested once a week in a group of male rats (n = 132)
from the 24th month of their life. Because of the age-related
decay of this function none of the 2-year-old animals
displayed full scale sexual activity. By dividing the
group equally the rats were treated with saline (1 ml/kg,
s.c.) and Deprenyl (0.25 mg/kg, s.c.), respectively,
three times a week. In the saline-treated group (n =
66) the last signs of sexual activity vanished to the
33rd week of treatment. (-)Deprenyl treatment restored
full scale sexual activity in 64 out of 66 rats. The
longest living rat in the saline-treated group lived
164 weeks. The average lifespan of the group was 147.05
+/- 0.56 weeks. The shortest living animal in the (-)Deprenyl-treated
group lived 171 weeks and the longest living rat died
during the 226th week of its life. The average lifespan
was 197.98 +/- 2.36 weeks, i.e. higher than the estimated
maximum age of death in the rat (182 weeks). This is
the first instance that by the aid of a well-aimed medication
members of a species lived beyond the known lifespan
maximum.
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Radioisotope Research Institute,
Faculty of Medicine, University of Tokyo, Japan.
(-)Deprenyl, a MAO-B inhibitor
that is also known to be effective for symptoms of Parkinson's
disease, when injected subcutaneously (sc) in male Fischer-344
rats at a dose of 0.5 mg/kg per day (3 times a week)
from 18 months of age, significantly increased the remaining
life expectancy. The average life span after 24 months
was 34% greater in treated rats than in saline-treated
control animals. Furthermore, a short-term (3 wk) continuous
sc infusion of Deprenyl significantly increased activities
of superoxide dismutase and catalase but not of glutathione
peroxidase in selective brain regions such as s. nigra,
striatum, and cerebral cortex, but not in hippocampus
or cerebellum, or the liver. The optimal dose for increasing
these activities, however, differed greatly depending
on the sex and age of animals, with a 10-fold lower
value for young female than male rats. Interestingly,
aging caused an increase and a decrease in the optimal
dose in female and male rats, respectively. In addition,
treatment for a longer term tended to reduce the optimal
dosage in the same animal group. The results clearly
demonstrate that Deprenyl increases antioxidant enzyme
activities in selective brain regions. If this effect
of Deprenyl is causally related to its life-prolonging
effect, the dosage to be used for any life span study
would be a critical factor, with the dosage differing
widely depending on sex, age of animal, and mode and
duration of drug administration.
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Department of Pharmacology, Semmelweis
University of Medicine, Budapest, Hungary.
Six months old ovariectomized
female rats (n = 9) were treated with (-)Deprenyl in
a dose of 0.25 mg/kg s.c. three times a week, and (n
= 9) with physiologic saline (0.1 ml/100 g) till decay.
It was found that control females (n = 9) decayed within
the age of fifteen months while the members of the (-)Deprenyl
treated group were all alive at that age. Moreover three
(-)Deprenyl treated female rats reached 36 months of
age. Sexual activity was quite absent in both groups.
The data suggests that (-)Deprenyl extended the lifespan
of female rats only in total absence of gonadal hormones
and sexual activity.
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National Institute for Longevity
Sciences, 36-3, Gengo, Morioka-cho, Obu-shi, 474-8522,
Aichi, Japan.
(-)Deprenyl, a monoamine oxidase
B (MAO B) inhibitor is known to upregulate activities
of anti-oxidant enzymes such as superoxide dismutase
(SOD) and catalase (CAT) in brain dopaminergic regions.
The drug is also the sole chemical which has been repeatedly
shown to increase life spans of several animal species
including rats, mice, hamsters and dogs. Further, the
drug was recently found to enhance anti-oxidant enzyme
activities not only in brain dopaminergic regions but
also in extra-brain tissues such as the heart, kidneys,
adrenal glands and the spleen. We and others have also
observed mobilization of many humoral factors (interferone
(INF)-gamma, tumor necrosis factor (TNF)-alpha, interleukine
(IL)-1beta,2,6, trophic factors, etc.) and enhancement
of natural killer (NK) cell functions by (-)Deprenyl
administration. An apparent extension of life spans
of experimental animals reported in the past may be
better explained by these new observations that (-)Deprenyl
upregulate SOD and CAT activities not only in the brain
but also in extra-brain vital organs and involve anti-tumorigenic
as well as immunomodulatory effect as well. These combined
drug effects may lead to the protection of the homeostatic
regulations of the neuro-immuno-endocrine axis of an
organism against aging.
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