Brain Lightning™
The only
Nootropic you will ever need!
Brain
Lightning™ Rocks Fall 1999 ACAM Conference!
During the weekend
of October 29, 30 and 31st, the Fall 1999 Conference of the American
College for the Advancement in Medicine was held at the Hilton
in Reno, Nevada. Unveiled and launched at the conference, the profound
new brain/memory/IQ enhancement formula Brain Lightning™ got the attention
of a host of doctors, biochemists and other professional attendees,
who acquired information on the capabilities and scientific background
of the product and sampled the product themselves. Virtually all the
attendees who explored Brain Lightning™ left the conference with a
new appreciation of neurochemistry, were profoundly excited about
the prospects Brain Lightning™ represented for neurological protection
and health, and those who tried the product were visibly impressed
with the increase in clarity and focus experienced during their day
at the conference
Celebrate
the Millennium with a Working Brain!
Would you like to stop feeling brain fogged? Suffering too
many neurological deficits from living on a polluted planet? Losing
concentration, focus and ability to remember things? Concerned about
reduced atmospheric oxygen levels? Surrounded by too many organophosphates
and nerve toxins?
Need Optimum Brain Function in spite of yourself
and your environment? Tired of watching others advance ahead of you
on the job or in school?
Optimize
Your Focus, Memory and Concentration with
Brain Lightning™
The Ultimate High Performance Neurological Supplement!
Brain
Lightning™
Where
the hype stops and performance begins!
The only Nootropic you will ever need!
Would you like to stop feeling brain fogged?
Suffering too many neurological deficits from living on a polluted
planet?
Losing concentration, focus and ability to remember things?
Concerned about reduced atmospheric oxygen levels?
Surrounded by too many organophosphates and nerve toxins?
Do you find yourself in a stress-filled environment and can't afford
to lose concentration?
Need
Optimum Brain Function in spite of yourself and your environment?
Tired of watching others advance ahead of you on the job, in school
or in the field?
About Brain Lightning™
Brain Lightning™ is a brand new
synergistic neurological supplement which exceeds
the capabilities of virtually every product available on the planet.
The outstanding features of Brain Lightning™
include:
Promotes fast, accurate thought processes.
Promotes better short-term and long-term memory.
Promotes enhancement of intelligence capability and neural processing.
Promotes enhanced concentration and focus.
Protects against age-related cognitive decline.
Improves glucose and oxygen utilization in the brain.
Increases mental energy, memory recall and mental sharpness.
Facilitates cerebral metabolism and detoxification processes.
Enhances blood flow to the brain.
Alleviates symptoms related to glaucoma and improves vision.
Increases acetylcholine concentration.
Aids in the prevention of organophosphate pesticide toxicity.
Aids in the prevention of nerve gas toxicity (US Army currently investigating
the benefits of Huperzine A for this purpose) and orthophosphate pesticide
exposure toxicity.
Improves auditory and visual capability.
All ingredients in Brain Lightning™ have
been shown by many studies to be profound neurological and memory
enhancers. This synergistic formulation contains a proprietary blend
of the leading nootropic nutrients available, to create a powerful,
effective neurological supplement. Brain Lightning™
is a proprietary, synergistic blend of Huperzine A,Vinpocetine, Trimethylglycine
(TMG), DL Phenylalanine, GABA, DMAE, L-Tyrosine, Gingko Biloba, Pregnenolone,
supported by Magnesium, Thiamin, Pantothenic Acid, Vitamin B6 (as
Pyridoxine 5 Phosphate), Niacin (non-flushing, as niacinamide), Vitamin
B12 (as Cyanocobalamin and Selenium (as selenium chelate). These ingredients
are synergistically blended in thresholds guaranteed to be both safe
and effective, unlike some other nootropic products on the market.
There is little "biological noise" with Brain Lightning™, compared
to choline-based formulae. Our formulation is yeast
free and fluoride free.
Contraindications: This product is NOT
intended for children, people with PKU (phenylketonuria), or pregnant/lactating
women. If you have high bloodpressure, hemophilia, heart problems,
pre-existing pigmented malignant melanoma, migraine headaches , or
are taking blood thinning medication or other prescription drugs,
use only under the guidance of a physician. Do NOT take this formulation
with MAO inhibitor anti- depressants.
Suggested Use: As a dietary supplement,
take one to three capsules daily to acheive the optimum neuro-physiological
effect. Take with light non-protein food, followed by two glasses
of water. There are 15 mg of Vinpocetine and
60 mcg of pure un-synthesized Huperzine A in each 3 cap serving.
Ingredients in Brain Lightning™ Serving
of 3 tablets provides:
Vitamin E, natural,
(d-alpha tocopherol) Essential for neural memory functions. The natural
Vitamin E may also play a role in delaying Alzheimer's. Anti-oxidant
functions. 100 IU 333%
Vitamin B-1 ( Thiamin) Promotes health in nerve cells, the brain and
the heart by promoting neural metabolism processes. 25 mg 1667%
Vitamin B-3 (Niacin, non-flushing, as niacinamide) Enhances utlization
of GABA. Reduces plasma fibrinogen and low-density lipoprotein cholesterol.
10mg 50%
Vitamin B-5 (Pantothenic Acid) Promotes synthesis of hormones and
neurotransmitters 25mg 250%
Vitamin B-6 (Pyridoxine 5- Phosphate) Enhances utilization of Phenylaline
and GABA components 25mg 1250%
Vitamin B-12 (as Cyanocobalamin ) Promotes nervous system function
and DNA synthesis. 250mcg 4167%
Magnesium Reduces neuromotor impairment and deficit. Anti-aging capabilities.
Aids in the transmission of nerve impulses. 50mg 13%
Zinc (as Amino Acid Chelate) Essential for maintaining ionic channels
and cognitive function. The presence of Zinc aids in the production
of over 300 enzymes, many of them in the brain. 10mg 67%
Manganese (as Manganese Chelate) Trace needed for brain and nerve
function, and necessary for the absorption of Vitamin B-1 and Vitamin
E. 5mg 250%
Selenium (as Amino Acid Chelate) Important for Thyroid function. Anti-oxidant.
Prevents breakdown of Vitamin E. 200mcg 286%
Magnesium Silicate, Calcium Carbonate, Silicon Dioxide, Cellulose
(non-reactive mixing agents)
Proprietary Synergistic
Blend of Brain Nutrients found only in Brain
Lightning™
DMAE (dimethylaminoethanol)
Reduction of anxiety and hyperactivity, precursor to Acetylcholine,
increase in intellectual capacity, learning ability, sensory functions,
reduction of hyperactivity and anxiety, mood stabilization, increases
short and long-term memory functions, and more.
PREGNENOLONE Cumulative anti-stress, anti-aging and anti-fatigue effects
for the brain. Improves spatial memory, verbal recall, precursor to
all steroid hormones, lowers excessive GABA activity, promotes body
de-toxification processes, and more.
TRIMETHYLGLYCINE (TMG) Lowers homocysteine levels, stops DNA replication
error, functions as a precursor for the formation of SAMe, a critical
factor in biochemical reactions.
L-TYROSINE Prevents reduction of noropinephrine levels associated
with stress, associated with a reduction in emotional depression,
functions as a precursor to Thyroxine (primary thyroid hormone), as
well as adrenaline and noradrenaline. HUPERZINE A (natural) Protects
brain cells against glutamate-induced excitotoxicity, inhibits ACHe,
and lowers liver toxicity. Huperzine A actually promotes the growth
of nerve dendrites!
VINPOCETINE Increases cerebral blood flow, increases production of
ATP for cellular energy, increases use of oxygen and glucose in brain
cells, raises serotonin level in the brain and neural information
processing rate, dramatic increase in memory functions. D,L,
PHENYLALANINE Blocks breakdown of enkephalins, aids in depression,
precursor for Tyrosine, promotes mental alertness, elevates mood,
and more. GABA (gamma aminobutyric acid) Aids in production of relaxed
mental state, prevents neural overload conditions. Balanced by Pregnenlone,
which blocks excessive GABA activity.
GINGKO BILOBA Improves blood flow to the brain and subsequent oxygenation
of brain cells, promotion of cellular metabolism, increases cellular
glucose utilization, and more.
Function of Ingredients in Proprietary
Blend
DMAE: DMAE (dimethylaminoethanol)
is naturally present in small amounts in the human brain, and is found
naturally in some foods, like anchovies and sardines. It is a precursor
(building block) to Acetylcholine, a major brain neurotransmitter,
which of course readily crosses the blood-brain barrier. Research
indicates that supplementary DMAE promotes neurological processes
which result in increased intellectual capacity,
increased learning capability, increased short and long-term memory
capability, promotes concentration, focus and alertness, and improves
general sensory capabilities (vision, hearing, etc.) DMAE also contributes
to the reduction of anxiety and hyperactivity, and contributes to
stable behavior and mood. DMAE is part of the "choline cycle",
which allows cells to convert certain specific biochemicals into each
other as needed. One of the key roles for choline is as the rate-limiting
factor in the production of acetylcholine. Acetylcholine is one of
the dozen or so major neurotransmitters which allow brain and nerve
cells to communicate with each other. Acetylcholine-using neurons
are especially important in: (1) cognitive (intellectual) function;
(2) memory formation and emotional modulation; and (3) the reticular-activating
system (RAS). The RAS is a group of nerve clusters which sits at the
top of the spinal cord and acts as a "traffic controller". The RAS
determines what stimuli from the senses will be allowed to reach conscious
attention, as well as what thoughts and feelings will be allowed to
initiate corresponding bodily movements. It is partly due to the RAS
that a passing angry thought or feeling doesn't automatically and
instantaneously trigger violent behavior toward the object of our
anger. It is the intensity of signals (mediated by DMAE- derived acetylcholine)
from the RAS to the hippocampus and cerebral cortex which determines
the intensity and duration of sustained mental focus and attention
- the very issue at the root of genuine attention deficit disorder.
Thus DMAE, by being the most effective precursor for brain/RAS acetylcholine,
literally increases attention span, mental focus, and ability to screen
out distracting and extraneous stimuli (both from the environment
as well as from within). An acetylcholine-deficient RAS will have
a difficult time maintaining a high level of focus, attention, alertness
and arousal. DMAE is the most effective acetylcholine precursor for
several reasons. Choline salts (e.g. choline bitartrate, choline chloride,
choline citrate) are frequently broken down by bacteria living in
our gut. DMAE does not suffer this fate. What choline is absorbed
into the bloodstream has a poor ability to cross the blood-brain barrier.
The blood-brain barrier is a two-part barrier which prevents toxins
from entering the brain and also prevents disruptions of brain function
due to surges in the blood of various nutrients, even those essential
for optimum brain function. Unlike choline, DMAE passes easily through
the blood-brain barrier. Because of this fact, DMAE has been shown
to be effective at doses as low as 10-20 mg, although doses of 500-1000
mg are often needed. The unique effectiveness of DMAE is also due
in part to its ability to inhibit choline oxidase, an enzyme which
can divert choline away from acetylcholine production, into betaine
production instead. And while a third acetylcholine precursor, phosphatidylcholine,
is more effective than simple choline salts, studies have found large
(and expensive) doses - 10 to 60 grams(!) - are often needed to elevate
brain acetylcholine levels. Many other products on the market rely
on phosphatidylcholine, which is not as effective as DMAE.
PREGNENOLONE: PREGNENOLONE is
a precursor for all other steroid hormones naturally present in the
body. It is converted directly into DHEA, which in turn converts to
testosterone, estrogens, cortisol and aldosterone. It is this same
set of successive conversions that makes human life possible. Without
the presence of Pregnenolone, there can be no human steroid production.
Research into Pregnenolone with factory workers and pilots began in
the 1940's, and the evidence rapidly materialized that Pregnenoline
had energizing and cumulative anti-stress, anti-fatigue
and anti-depression effects, especially after it was taken
after a period of two weeks. Studies at St. Louis School of Medicine
showed the memory enhancement effects
of pregnenolone, with improvement in spatial
memory, perception and verbal recall. There is considerable
evidence that pregnenolone modulates both NMDA
and GABA receptors systems in the brain (which are involved
in learning, memory and alertness and decrease with age). Pregnenoline
enhances NMDA receptor function and lowers excessive GABA activity
and seems to be a natural anti-depressant.
During research conducted in the 1940's, it was found pregnenolone
use resulted in a reduction in joint pain - it was used as a treatment
for arthritis, but it was replaced by Cortisone in the 1950's. The
body produces a steroid called cortisol, the levels of which increase
with age, causing a number of problems. Pregnenolone counteracts
the negative effects of accumulating cortisol levels in the body,
including the enhancement of memory areas in the brain damaged by
cortisol. One of the major determinants of the body's ability to detoxify
poisonous chemicals is the health and effectiveness of the Cytochrome
P450 enzyme system in the liver. Pregnenolone increases the overall
P450 detox enzyme power of the liver by promoting conservation of
the existing enzymes, promoting body detoxification
processes. Works with TMG, detailed below.
TRIMETHYLGLYCINE (TMG): TRIMETHYLGLYCINE
is what is called a methylation agent, composed of three methyl groups
attached to one molecule of the amino acid glycine. It produces unique
biological effects including lowering general
homocysteine levels in the blood. Homecysteine is thought to
contribute toward strokes and cardiovascular disease. TMG also contributes
one of its methyl groups to DNA, potentially reducing
DNA aging and errant DNA replication processes. In order for
TMG to be effective in the body, it needs to have the synergistic
co-factor of Vitamin B12, which is also included in the Brain Lightning™
formulation. Trimethylglycine also produces
other compounds in the body, such as SAMe (S- Adenosylmethionine.
SAMe is an active lipotrope form of Methionine, and is a cofactor
in a number of critical biochemical reactions and is found in almost
every tissue of the body. SAMe has been used in clinical studies to
treat depression, schizophrenia, demyelination diseases, liver disease,
dementia, arthritis, peripheral neuropthy and other conditions. Several
studies have confirmed that SAMe is up to15% more effective in the
treatment of depression than traditional pharmaceutical anti-depressants.
SAMe improves and normalizes liver function. SAMe is used in Europe
in the treatment of cirrhosis and damage caused by alcohol. SAMe is
essential for the production of glutathione, a powerful antioxidant
that protects the body from the damaging effects of free radicals.
SAMe reduces the number of trigger points, reduces fatigue, reduces
morning stiffness,and improves mood in fibromyalgia patients. SAMe
improves the binding of neurotransmitters to their receptors sites
in the brain. SAMe is essential for the regeneration of neuron axons
following injury. SAMe is also essential for the formation of myelin
sheaths that surround axons. In tests SAMe has shown great promise
in the treatment of Peripheral Neuropathy, and HIV related peripheral
Neuropathy. Alzheimer's and Parkinson's patients have very low levels
of SAMe. SAMe is currently under investigation as a treatment for
Parkinson's disease.
L-TYROSINE: Tyrosine is intimately
involved with the important brain neuro- transmitters epinephrine,
norepinephrine and dopamine. It is synthesized in the body from existing
levels of phenylalanine. Environmental stress is associated with reduced
levels of norepinephrine. Tyrosine prevents
reduction of norepinephrine levels that are associated with stress.
Many clinical studies, along with a large body of anecdotal evidence,
indicate that tyrosine may prove to be a vital
substance in alleviating depression, as well as the irritating
symptoms of premenstral syndrome. Tyrosine is now reportedly being
used as an aid in the treatment of and withdrawal from cocaine addiction.
In one study, tryptophan and tyrosine were used in conjunction with
the anti-depressant imipramine to treat chronic cocaine abuse with
a reported 75-80 percent success rate. Researchers at UCLA and elsewhere,
have also reported favorably on regimens containing tryptophan and
tyrosine for the treatment of cocaine abuse. The importance of Tyrosine
is based on the fact that it is a direct precursor to Thyroxine (Triiodo
tyrosine) as well as being a precursor to Adrenaline and Noradrenaline.
Thyroxine is, of course, a primary Thyroid hormone. Thyroxine deficiency
results in a series of conditions including excess weight gain, cold
hands and feet, decreased basal metabolism, etc.The catecholamine
Adrenaline and Nor Adrenaline are critical in the following conditions:
In Science magazine it was reported that Tyrosine lowers blood pressure
by increasing Norepinephrine metabolites which through feedback shut
down sympathetic output. In this same issue it was found that Tyrosine
increased blood pressure 38% to 49% in hypotensive rats through accelerated
peripheral synthesis of catecholamine. A study by Dr. I. Goldberg
in Lancet revealed that catecholamine also controls immune system
output. Allergy sufferers have responded well to Tyrosine. In the
American Journal of Psychiatry, Dr. Alan J. Gelenberg postulated that
a lack of available tyrosine results in a deficiency of nor adrenaline
at a specific brain location, which in turn relates to mood problems
such as depression.
HUPERZINE A: An amazing, safe
alkaloid derived from the Chinese Club Moss, Huperzia serrata, Huperzine
occurs in two forms: Huperzine A and Huperzine B, which has far less
effect than Huperzine A. Double blind studies in China have demonstrated
the positive effects of Huperzine A for the treatment of Alzheimer's
Syndrome. It is currently approved for AD treatment in China. Huperzine
A appears to relieve symptoms of Alzheimer's disease by blocking the
depletion of acetylcholine in the brain. Huperzine A is currently
under study by the US Army at Walter Reed Hospital as an antidote
for nerve gas poisoning because of its protective effect on the cells
of the brain. Huperzine A actually promotes the growth of nerve dendrites!
Animal and cell culture studies, along with molecular structure data,
suggest that Huperzine A is a potent acetylcholinesterase (AChE) inhibitor
and may also protect neurons against glutamate-induced
excitotoxicity. The molecule's strong specificity for AChE
suggests it may lower liver toxicity and other adverse effects. Huperzine
A costs approximately $500,000 per Kilo, because they have to gather
it molecule by molecule. Brain Lightning™ uses
only natural Huperzine A, as opposed to some formulations on
the market which use synthetic Huperzine A. For more data, see this
link. In orthodox medicine, there are two phamaceuticals
used in the treatment of Alzheimers, tacrine and physostigmine, both
of which unfortunately bind to receptors in the central nervous system,
causing adverse effects. Also, the two orthodox drugs work on the
AChE everywhere in the body instead of just in the brain, so their
effect is severely limited. Huperzine A specifically targets the AChE
in the brain, does much better in improving memory, does not bind
to CNS receptors, and lasts more than ten times longer. Huperzine
A is not known to have any toxicity at all, even at doses 100 times
the therapeutic dose. Tens of thousands of people, if not more (considering
China) have used Huperzine A with no evidence of toxicity anywhere
in the body. See studies below
VINPOCETINE: Vinpocetine is
more technically referred to as "ethyl apovincaminate." Derived from
the periwinkle plant, Vinpocetine, a derivative of Vincamine, increases
cerebral blood flow, increases the rate at which brain cells produce
Adenosine TriPhosphate (ATP), creating more cellular energy, and increases
the use of oxygen and glucose, feeding the brain cells. It also has
the unusual effect of raising the level of serotonin in the brain,
increasing the general brain information processing rate. It is commonly
cited as an aid to improving memory. Literature suggests Vinpocetine
may act to improve conditions related to insufficient blood flow to
the brain including vertigo and Meniere's syndrome, difficulty in
sleeping, mood changes and depression. Vinpocetine may also alleviate
speech impairment, improve short-term memory, hearing, assist in the
condition of multiple infarct dementia, increase resistance of neurons
to lack of oxygen. Several brain boosters (ginkgo biloba, vitamin
E, phosphatidylserine, to name just a few) are known to help restore
failing memory, but Vinpocetine dramatically enhances memory even
in healthy individuals. It also acts as a potent neuroprotective supplement.
Strong clinical evidence exists that, in addition to its brain boosting
properties, Vinpocetine's ability to improve blood flow also helps
protect brain and heart function, prevents macular degeneration (a
leading cause of blindness in the elderly), and improves hearing and
inner ear problems, and even lessens depression and fatigue. See
studies below
DL-PHENYLALANINE: Most amino
acids, with the exception of glycine, can appear in two forms called
the D- and L- forms. Each form is a reversed mirror image of the other.
Amino acids in the L- form are the natural form of amino acids found
in living plant and animal tissues, and are considered to be more
compatible to human biochemistry than the D- forms. All amino acids
used in human protein structures are of the L- form, with the exception
of phenylalanine, which can also appear as DL-phenylalanine. Phenylalanine
comes in two forms which are mirror images of each other: L-phenylalanine
which has a nutritional value, and D-phenylalanine which has painkilling
and depression alleviating properties which are attributed
to its ability to block the breakdown of enkephalins, the brains natural
pain killers. A third form, DL-phenylalanine, is a 50/50 mixture of
these two forms. Phenylalanine activity is enhanced
by additional Vitamin B6, especially in studies on depression. Vitamin
B6 is, of course, included in Brain Lightning™.
Phenylalanine deficiency can cause bloodshot eyes, cataracts and behavioral
changes. It is one of the amino acids which the body cannot manufacture
itself, but must acquire from food. It is abundant in meats and cheese.
Phenylalanine is a precursor of tyrosine, and together they lead to
the formation of thyroxine or thyroid hormone, and of epinephrine
and norepinephrine which is converted into a neurotransmitter used
by the brain to manufacture norepinephrine which promotes mental alertness,
memory, elevates mood, and suppresses the appetite very effectively.
GABA: GABA (gamma aminobutyric
acid), is an important amino acid which functions as the most prevalent
inhibitory neurotransmitter in the central nervous system. GABA's
high concentration in the hypothalamus suggests this amino acid plays
a significant role in hypothalamic-pituitary function. The hypothalamus
is a region of the posterior section of the brain and is the regulating
center for visceral (instinctive) functions such as sleep cycles,
body temperature, and the activity of the pituitary gland. Supplemental
GABA can be useful in producing a state of relaxation. GABA works
in partnership with a derivative of Vitamin B-6 (Pyridoxine - included
in Brain Lightning™), to cross from the
axons to the dendrites through the synaptic cleft, in response to
an electrical signal in the neuron and inhibits message transmission.
This helps control the nerve cells from firing too fast, which would
overload the system. The action of GABA decreases epileptic seizures
and muscle spasms by inhibiting electrical signals in this manner.
Studies have shown that the site of action in the brain of benzodiazepams,
including Valium, is directly coupled to the brain receptor for GABA.
GABA itself can be taken instead of a tranquilizer to calm the body
without the fear of addiction. Taken with the B-vitamins niacinamide
and inositol, it prevents anxiety messages from reaching the motor
centers of the brain by filling its receptor site.
GINGKO BILOBA: The primary causes
of mental deficiencies is poor blood flow to the brain or "cerebral
vascular insufficiencies." An answer to this problem may come from
a plant which has been used for medicinal purposes since 2800 B.C.
It is found in the oldest Chinese books on herbal medicine, known
as materia medicas. The plant may provide the most important medicinal
plant extract available as we enter a new millennium-nearly 5000 years
later. The plant is Ginko biloba. Ginkgo works in a number of important
ways to assist the brain. The effect of the plant on cerebral vascular
insufficiency has been widely studied. An analysis of forty of the
scientific articles reporting on this subject noted ginkgo's clear
value in treating the "symptoms of aging" in the elderly. The studies
looked at an extract of ginkgo which was standardized for the level
of Ginkgo flavonglycosides. The active principles of Ginkgo extract
are believed to have a regulating effect on the entire vascular system
of veins, arteries and capillaries. Ginkgo extract may inhibit "Platelet
activating factor" (PAF) and promote the metabolism of cerebral and
neurosensorial cells. The most common usage of Gingko Biloba is for
its widely accepted effects in the regulation of blood flow to the
brain, legs and other extremities. It is also thought Gingko Biloba
may act to counteract a number of conditions such as vascular insufficiency
or tinnitus. Gingko Biloba has also been indicated in the treatment
of intermittent claudication (pain while walking). Ginkgo not only
assists the brain by increasing its supply of blood and oxygen, but
also this plant has been shown to increase ability of brain cells
to make use of glucose. Energy production is improved. Nerve signal
transmissions are improved. Brain wave tracings are improved. Diverse
population grouping have been shown to benefit from administration
of ginkgo. The memory of college students as well as the elderly have
shown improvement. Ginkgo facilitates short-term memory by increasing
the speed of nerve impulses. In recent years, this plant has reached
a highly valued status in Europe. In France, 1.5 percent of all prescription
sales are for ginkgo leaf extract. The figure is 1 percent in Germany.
In both of these countries, the extracts of the ginkgo leaf are among
the leading prescription medicines. Worldwide, some 10 million prescriptions
for the extract this plant leaf were written in 1989; roughly 100,000
physicians prescribe ginkgo as a regular part of their practices.
If you were to purchase all these ingredients separately in the amounts
available in a bottle of Brain Lightning™, it would cost you more
than $110.00, and you still wouldn't be getting the purity of many
ingredients used in this product.
Order your Brain
Lightning™
today!!!
One (1) Bottle of 90 vegi-caps - $69.95
Three (3) Bottles, multiple discount at $59.95 each ($179.85).
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Research background on Huperzine A
:
Research conducted at the Weizmann Institute
of Science in Israel
"A moss extract that has been used for centuries in Chinese herbal
medicine to treat a range of symptoms from confusion and strain
to swelling and schizophrenia could hold the key to a new generation
of drugs for treating Alzheimer's disease (AD), according to researchers
at the Weizmann Institute of Science in Israel.
Mia Raves and her colleagues have determined the 3-D structure of
a complex formed between Huperzine A (HupA) a novel alkaloid extracted
from the club moss Huperzia serrata and the message-carrying brain
enzyme acetycholinesterase (AChE), which is thought to be involved
in AD. They found that the structure revealed a 'strikingly good fit
between HupA and the enzyme' and concluded that it may be a possible
starting point for designing 'a new generation of Alzheimer drugs
with improved properties'.
According to one theory, memory impairments and other cognitive defects
associated with AD patients result from the degeneration of nerve
cells which release the message-carrying acetycholine. The deficiency
of acetycholine in the brain that ensues is then compounded by the
action of AChE, which breaks down acetycholine in the body.
The scientists used high quality crystals of AChE derived from electric
organ tissue of the Torpedo fish (one of the richest sources of this
enzyme) and soaked the crystals with HupA (Nature Struct. Biol., January
1997, p 57). Using X-ray crystallography they obtained a 3-D computer
image of AChE-HupA binding. This revealed how the HupA blocks the
enzyme by sliding 'smoothly into the active site of AChE where acetylcholine
is broken down, and latches onto the site via a large number of subtle
chemical links'. The binding closes off the enzyme's cutting machinery,
thus protecting the acetylcholine.
Because the binding is very specific, says Professor Israel Silman,
a protein chemist at Weizmann, HupA 'could be a potent drug even when
used in small quantities', thus minimising the risk of side-effects.
Professor Joel Sussman, a crystallographer and one of the authors
of the study, commented: 'It is as if this natural substance were
ingeniously designed to fit into the exact spot in AChE where it will
do the most good'.
Several cholinesterase inhibitor (ChEI) drugs are already on the market,
including tacrine (Cognex), physostigmine (Phy), E2020 (Aricept) and
galanthamine, but these have significant limitations. For example,
tacrine has been associated with liver toxicity at high doses and
Phy has a short duration of action and low dosing range. The researchers
at the Weizmann Institute believe that HupA 'may serve both to alleviate
reduced AChE levels in the brain and to decrease neuronal cell death'
and they have reported positive results from clinical trials in China.
According to Professor Tang Xi-Can, of the Shanghai Institute of Materia
Medica, 'HupA has attracted considerable interest because of its unique
anti-AChE activity as well as memory-enhancing effects on a broad
range of behavioural models. HupA has good penetration through the
blood-brain barrier, high oral bioavailability and longer duration
of inhibitory action on AChE'. He described HupA as a 'novel Lycopodium
alkaloid which is chemically unique from other agents for AD (Asia
Pharmacol. Sini., November 1996, p 481).
By solving the structure of the 3-D complex, the researchers have
determined how AChE is blocked and hope to use this information to
design and analyse analogues of HupA with improved pharmacological
characteristics."
Other Research and Evaluation
Alzheimer's disease is characterized by abnormalities and degeneration
of neurons which depend upon acetylcholine and acetylcholine esterase
for normal activity and viability. These cells located in the basal
forebrain are also implicated in other neurological diseases such
as Parkinson's disease. Huperzine A is a potent inhibitor of acetylcholine
esterase, superior in activity to TACRINE, the first drug licensed
in the USA for Alzheimer's disease and E2020 which was licensed recently
by Eisai Pharmaceuticals. In addition, Huperzine A has been shown
to protect neuronal cells in culture from death caused by the excitoamino
acid glutamate. Because of the dual pharmacological action of Huperzine
A, provides a unique and important activity for the treatment of AD
and senile memory deficits.
Toxicology and efficacy studies of Huperzine A show it to be non-toxic
even when administered at 50-100 times the human therapeutic dose.
The extract is active for 6 hours at a dose of 2 µg/kg with no remarkable
side effects.
In Alzheimer's disease, double blind controlled studies of over 160
patients, showed significant improvement measured by Weschler scale
results, at doses of only 150 µg given twice daily (3-5 µg/kg).
Two important characteristics of Huperzine A distinguish it from TACRINE
and E2020 as well as other experimental compounds in development.
Huperzine A is highly specific for brain acetylcholine esterase (AChE)
vs. AChE found elsewhere in the body. This selectivity is believed
to be responsible for the relatively low toxicity of the extract.
In addition, unlike the two approved drugs for Alzheimer's disease,
TACRINE and E2020, Huperzine A has been shown to lack binding to receptors
in the CNS that can cause side effects such as the muscarinic receptors
M1 and M2.
The duration of action of Huperzine A at 3 hours is superior to TACRINE
(2 hours) and physostigmine (30 minutes). In behavioral experiments
of learning and memory enhancement in animals, the difference between
amounts of the extract effective for memory and learning and the no-toxic-effect
dose (from toxicity studies) was 30-100 fold. These data strongly
suggest that Huperzine A can be useful in treating Alzheimer's disease
with minimal side effects.
Research
Some Studies on Huperzine A:
Ashani, Y., Grunwald, J., Kronman, C. et al (1994) Roles of tyrosine
337 in the binding of Huperzine A to the active site of human acetylcholinesterase.
Mol Pharmacol 45: 555-560. Ashani, Y., Peggins, JO 3ed., Doctor, BP.
(1992) Mechanism of inhibition of cholinesterase by Huperzine A. Biochem
Biophys Res Commun 184: 719-726.
Cheng, DH., Ren, H., Tang, XC. (1996) Huperine A, a novel promising
acetylcholinesterase inhibitor. Neuroreport 8: 97-101.
Cheng DH, Tang XC. Comparative studies of huperzine A, E2020, and
tacrine on behavior and cholinesterase activities. Pharmacol Biochem
Behav 1998 Jun;60(2):377-86.
Fink, DM., Bores, GM., Effland, RC. et al (1995) Synthesis and evaluation
of 5-amino-5, 6, 7, 8-tetrahydroquinolinones as potential agents for
the treatment of Alzheimer's disease. J Med Chem 38: 3645-3651.
Geib, SJ., Tuckmantel, W., Kozikowski, AP. (1991) Huperzine A-a potent
acetylcholinesterase inhibitor of use in the treatment of Alzheimer's
disease. Acta Crystalogr C 47: 824-827.
Grunwald, J., Raveh, L., Doctor, BP. et al (1994) Huperzine A as a
pretreatment candidate drug against nerve agent toxicity. Life Sci
54: 991-997.
Guan, LC., Chen, SS., Lu, WH. et al (1989) Effects of Huperzine A
on eletroencephalography power spectrum in rabbits. Chung Kuo Yao
Li Hsueh Pao 10: 496-500.
Hanin, I., Tang, XC., Kindel, GL. et al (1993) Natural and synthetic
Huperzine A: effect on cholinergic function in vitro and in vivo.
Ann N Y Acad Sci 695:304-306.
Hao, XY., Gong, ZH., Qin, BY. (1988) Effects of Huperzine A on cholinesterase
isoenzymes in plasma of mice and dogs. Chung Kuo Yao Li Hsueh Pao
9: 312-316. (article in Chinese) Hi, QX., Yi, FH., Xi, CT. (1995)
Huperzine A ameliorates the spatial working memory impairments induced
by AF64A. Neuroreport 6: 2221-2224.
Kozikowski, AP., Miller, CP., Yamada, F. et al (1991) Delineating
the pharmacophoric elements of Huperzine A: importance of the unsaturated
three-carbon bridge to its AChE inhibitory activity. J Med Chem 34:
3399-3402.
Laganiere, S., Corey, J., Tang, XC. et al (1991) Acute and chronic
studies with the anticholinesterase Huperzine A: effect on central
nervous system cholinergic parameters. Neuropharmacology 30: 763-768.
Lallement, G., Veyret, J., Masqueliez, C. et al (1997) Efficacy of
hyperine in preventing soman-induced seizures, neuropathological changes
and lethality. Fundam Clin Pharmacol 11: 387-397.
Liu, MY. and Liu, HC. (1995) Intelligence promoting Chinese materia
medica. Chung Kuo Chung Hsi I Chieh Ho Tsa Chih 15: 59-61. (article
in Chinese)
Lu, WH., Shou, J., Tang, XC. (1988) Improving effect of Huperzine
A on discrimination performance in aged rats and adult rats with experimental
cognitive impairment. Chung Kuo Yao Li Hsueh Pao 9: 11-15. (article
in Chinese)
McKinney, M., Miller, JH., Yamada, F. et al (1991) Potencies and stereoselectivities
of enantiomers of Huperzine A for inhibtion of rat cortical acetylcholinesterase.
Eur J Pharmacol 203:303-305.
Pang, YP. and Kozikowski, AP. (1994) Prediction of the binding site
of 1-benzyl-4-[(5,6-dimethoxy-1-indanon-2-yl) methyl] piperidine in
acetylcholinesterase by docking studies with the SYSDOC program. J
Comput Aided Mol Des 8: 683-693.
Pang, YP. and Kozikowski, AP. (1994) Prediction of the binding sites
of Huperzine A in acetylcholinesterase by docking studies. J Comput
Aided Mol Des 8: 669-681.
Qian, BC., Wang, M., Zhou, ZF. et al (1995) Pharmacokinetics of tablet
Huperzine A in six volunteers. Chung Kuo Yao Li Hsueh Pao 16: 396-8
Raves, ML., Harel, M., Pang, YP. et al (1997) Structure of acetylcholinesterase
with the nootropic alkaloid, (-) -Huperzine A. Nat Struct Biol 4:
57-63.
Saxena, A., Qian, N., Kovach, IM. et al (1994) Identification of amino
acid residues involved in the binding of Huperzine A to cholinesterases.
Protein Sci 3: 1770-1778.
Skolnick AA. Old Chinese herbal medicine used for fever yields possible
new Alzheimer disease therapy. JAMA 277 (10): 776 (Mar 1997).
Tang, XC., Kindel, GH., Kozikowski, AP. et al (1994) Comparison of
the effects of natural and synthetic Huperzine-A on rat brain cholinergic
function in vitro and in vivo. J Ethnopharmacol 44: 147-155.
Tang, XC., Xu., H., Feng, J. et al (1994) Effect of cholinesterase
inhibition in vitro by Huperzine analogs. Chung Kuo Yao Li Hsueh 15:
107-110.
Tang, XC., De Sarno, P., Sugaya, K. et al (1989) Effect of Huperzine
A, a new cholinesterase inhibitor, on the central cholinergic system
of the rat. J Neurosci Res 24: 276-285.
Tang, XC., Han, YF., Chen, XP. et al (1986) Effects of Huperzine A
on learning and the retrieval process of discrimination performance
in rats. Chung Kuo Yao Li Hsueh Pao 7: 507-511. (article in Chinese)
Ved, HS., Koenig, ML., Dave, JR. et al (1997) Huperzine-A, a potential
therapeutic agent for dementia, reduces neuronal cell death caused
by glutamate. Neuroreport 8: 963-8.
Wang, YE., Feng, J., Lu, WH. et al (1988) Pharmacokinetics of Huperzine
A in rates and mice. Chung Kuo Yao Li Hsueh Pao 9: 193-196. (article
in Chinese)
Wang, YE., Yue, DX., Tang, XC. (1986) Anti-cholinesterase activity
of Huperzine A. Chung Kuo Yao Li Hsueh Pao 7: 110-113. (article in
Chinese)
Xiong, ZQ. and Tang, XC. (1995) Effect of Huperzine A, a novel acetylcholinesterase
inhibitor, on radial maze performance in rates. Pharmacol Biochem
Behav 51: 415-419.
Xiong, ZQ., Tang, XC., Lin, JL. et al (1995) Effects of isovaniHuperzine
A on cholinesterase and scioikanube-induced memory impairment. Chung
Kuo Yao Li Hsueh Pao 16: 21-25.
Xu SS, Gao ZX, Weng Z, Du ZM, Xu WA, Yang JS, Zhang ML, Tong ZH, Fang
YS, Chai XS, et al. Efficacy of tablet huperzine-A on memory, cognition,
and behavior in Alzheimer's disease. Chung Kuo Yao Li Hsueh Pao 16
(5): 391-395 (Sep 1995).
Yan, XF., Lu, WH., Lou, WJ. et al (1987) Effects of Huperzine A and
B on skeletal muscle and the electoenephalogram. Chung Kuo Yao Li
Hsueh Pao 8: 117-123.
Zhang, GB., Wang, MY., Zheng, JQ. et al (1994) Facilitation of cholinergic
transmission by Huperzine A in toad paravertebral ganglia in vitro.
Chung Kuo Yao Li Hsueh Pao 15: 158-161. (article in Chinese)
Zhang, RW., Tang, XC., Han, YY. et al (1991) Drug evaluation of Huperzine
A in the treatment of senile memory disorders. Chung Kuo Yao Li Hsueh
Pao 12: 250-252. (article in Chinese)
Zhi QX, Yi FH, XI CT. Huperzine A ameliorates the spatial working
memory impairments induced by AF64A. Neuroreport 6 (16): 2221-2224
(Nov 1995).
Zhu, XD. and Giacobini, E. (1995) Second generation choliesterase
inhibitors: effect of (L)-Huperzine-A on cortical biogenic amines.
J Neurosci Res 41: 828-835.
Zhu, XD. and Tang, XC. (1988) Improvement of impaired memory in mice
by Huperzine A and Huperzine B. Chung Kuo Yao Li Hsueh Pao 9: 492-497.
(article in Chinese)
Zhu, XD. and Tang, XC. (1987) Facilitatory effects of Huperzine A
and B on learning and memory of spatial discrimination in mice. Yao
Hsueh Hsueh Pao 22: 812-817. (article in Chinese)
Zhu, XZ. (1991) Development of natural products as drugs acting on
central nervous system. Mem Inst Oswaldo Cruz 86: 173-175.
Vinpocetine:
Note: Vinpocetine is more technically referred
to as "ethyl apovincaminate."
D. Sauer et al (1988) "Vinpocetine prevents ischaemic cell damage
in rat hippocampus" Life Sci. 43, 1733-39.
D. Hadjiev & S. Yancheva (1976) "Rheoencephalographic and psychological
studies with Ethyl Apovincaminate in cerebral vascular insufficiency"
AF(DR)28, 1947-50.
(A. Kaham & M. Olah (1976) "Use of Ethyl Apovincaminate in ophthalmological
therapy" AF(DR)28, 1969-72. (12). H. Olpe et al (1985) "Locus Coeruleus
as a target for psychogeriatric agents" Ann NY Acad Sci 444, 399-405.
B. Saletu & J. Grunberger (1985) "Memory dysfunction and vigilance;
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in the treatment of sensorineuronal impairment of hearing" AF(DR)28,
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controlled evaluation of the safety and efficacy of vinpocetine in
the treatment of patients with chronic vascular senile cerebral dysfunction."
J. Am Geriatr Soc 35, 525-30. (16). E. Otomo et al (1985) "Comparison
of vinpocetine with Ifenprodil Tartrate and Dihyroergotoxine Mesylate
treatment and results of long term treatment with vinpocetine." Curr
Ther Res 37, 811-21. (17). E. Cholnoky & L. Domok (1976) "Summary
of safety tests of Ethyl Apovincaminate" AF(DR)28, 1938-44.
Rischke R, Krieglstein J. "Protective effect
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Kiss B, Karpati E. "Mechanism of action of vinpocetine." Acta Pharm
Hung 66(5):213-24, Sep 1996.
Miyazaki, M. "The effect of a cerebral vasodilator, vinpocetine, on
cerebral vascular resistance evaluated by the Doppler ultrasonic technique
in patients with cerebrovascular diseases." Angiology 46(1):53-8,
Jan 1995.
Tohgi, H., Sasaki, K. Chiba, K., Nozaki, Y. "Effect of vinpocetine
on oxygen release of hemoglobin and erythrocyte organic polyphosphate
concentrations in patients with vascular dementia of the Binswanger
type. Arzneim-Forsch 40(I), 6, 640-643, Jun 1990.
B. Vamosi et al (1976) "Comparative study of the effect of Ethyl Apovincaminate
and Xanthinol Nicotinate in cerebrovascular diseases" Arzneim Forsch
(drug research) 28, 1980-84. Hereafter abbreviated "AF (DR)")
F. Solti et al (1976) "Effect of Ethyl Apovincaminate on the cerebral
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E. Karpaty & L. Szporny (1976) "General and cerebral harmodynamic
activity of Ethyl Apovincaminate" AF(DR)28, 1908-12.
A. Szobor and M. Klein (1976) "Ethyl Apovincaminate therapy in neurovascular
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D. Sauer et al (1988) "Vinpocetine prevents ischaemic cell damage
in rat hippocampus" Life Sci. 43, 1733-39.
R. Branconnier (1983) "The efficacy of the cerebral metabolic enhancers
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DMAE:
Sergio W. Use of DMAE (2-dimethylaminoethanol) in the induction of
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Pregnenolone
The role of pregnenolone and its enhancement of memory function are
being explored with very interesting and promising results. The Geriatric
Research Education and Clinical Center in St. Louis, Missouri is one
of the world's leading research centers on pregnenolone. A 1995 study
conducted at the Center suggested that low levels of steroid hormones
might be the cause of learning and memory impairment (Flood et al.,
1995). They also did a study in 1992, which found a relationship between
pregnenolone levels in aging and the increase of cancer, and behavioral
disorders in people whom receive drugs that block the synthesis of
cholesterol (the precursor of pregnenolone) (Flood et al., 1992).
The National Institute of Mental Health in Bethesda, Maryland also
supports that pregnenolone is important for effective memory. The
NIH study found that pregnenolone positively modulates NMDA receptors
in the brain, which are believed to be responsible for retention (Mathis
et al., 1994). A French research study in 1995 found that when they
administered a series of cognitive tests to mice, those with the highest
steroid hormone levels performed significantly better (Rebel et al.,
1995). In addition to memory, serum levels of pregnenolone are also
a factor in depression. The NIH found that people with clinical depression
have significantly lower levels of pregnenolone. Pregnenolone levels
were decreased in subjects with affective illness, particularly during
episodes of active depression (Mathis et al., 1994).
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