| Enhancing Cognitive Function
|
2000-05-01 Ivy Greenwell – Lef.org
First, the bad
news: Doctors have confirmed that aging-related mental decline is
faster and more profound than originally believed. A new British
study of people over age 74 shows there is undeniable evidence of a
steep mental decline. The director of the study, Dr. Carol Brayne of
the Institute of Public Health in Cambridge, U.K. stated: "Although
we would prefer that aging not necessarily be accompanied by
cognitive decline, these data suggest that for the vast majority of
(elderly) populations, it is."
The good
news is the exciting finding that the brain can generate new neurons.
After decades of believing that neurons can only be lost with age,
scientists at Princeton have recently demonstrated that new nerve
cells are indeed being created in the brains of monkeys. The new
neurons are formed deep in the brain near the ventricles, then
migrate to various areas, including the prefrontal cortex, regarded
as the seat of "higher cognitive functions." The
implication of this discovery is that neurons (brain cells) can at
least be partly replaced. The old dogma held that the brain
inevitably shrinks and progressively atrophies as we age. Now this
dismal view can be discarded in favor of a new search for ways to
help the brain regenerate and preserve its youthful powers. If the
synthesis of new neurons takes place in human brains as well, and
everyone thinks it does, there is great hope for reversing brain
damage and preserving good cognitive function well into old age. The
new discovery also points to the importance of providing the brain
with the right nutrients, so that the new cells can be easily formed.
It would appear that neuronal regeneration is facilitated when there
is an abundance of cell membrane building blocks such as phosphatidyl
choline and phosphatidyl serine. Considering that nerve growth
factors are under hormonal control, adequate sex-steroid hormone
replacement is also an important consideration. Age-related cognitive
decline becomes noticeable in middle age, when people typically start
complaining that their memory isn't as good as it used to be. Past
the age of 50 or so, mental fitness, like physical fitness, has to be
consciously worked at. Raising the declining levels of
neurotransmitters is one challenge. The other is to maintain
efficient neural cell membranes with optimal fluidity.
Why we need
choline
The brain has a
voracious appetite for choline. There are two main reasons for the
brain's huge need for this nutrient: choline is required for
synthesis of the key neurotransmitter acetylcholine, and it is used
for the building and maintenance of brain cell membranes.
Acetylcholine is vital for thought, memory and sleep, and is also
involved in the control of movements. Not surprisingly, the
production of acetylcholine decreases with age, resulting in poor
memory, diminished learning ability and cognitive decline in general.
In Alzheimer's disease, the levels of acetylcholine are abnormally
low. It is the cholinergic neurons that show the most degeneration as
Alzheimer's disease progresses. When the brain does not receive
sufficient choline to manufacture acetylcholine, it may resort to
extracting choline out of the nerve cell membranes. This is called
auto-cannibalism. While in the short run this process provides a
supply of choline to produce enough acetylcholine to keep memory and
other brain functions going, in the long run the nerve cells become
badly damaged as neural cell membranes grow rigid and increasingly
dysfunctional. Choline is also important for the building of healthy
cell membranes. As phosphatidyl choline, it constitutes one third of
the cell membrane phospholipids. Phosphatidyl choline also serves as
the substrate, an enzyme that activates the formation of other
signaling neuro-chemicals.
Choline and
sleep
One of the
lesser-known functions of acetylcholine is helping to maintain sleep.
Acetylcholine controls the amount of sensory input. It strengthens
the so-called stimulus barrier, making it possible to sleep through
minor noises and other disturbances. As we age, we tend to become
"light sleepers," easily roused from sleep. Menopausal
women, who experience a sudden drop in acetylcholine levels due to
estrogen withdrawal, often complain about having suddenly become
"light sleepers." The same stimulus barrier also helps us
concentrate and solve problems. Too little acetylcholine makes us
distracted and irritable as too many unimportant stimuli bombard us,
in essence preventing us from thinking. Menopausal women who are
not on hormone replacement also tend to complain about the dryness of
their mucous membranes, which leads to problems such as nosebleeds.
Again, it is acetylcholine that keeps the mucous membranes moist. The
bladder too is under cholinergic control.
Choline helps
facilitate youthful methylation
The role of choline in
methylation probably explains the finding that choline-deficient
diets are associated with an increased rate of cancer in animal
studies. Dr. Craig Cooney, an expert in the field of methylation,
suggests that choline may in fact turn out to be important in the
treatment of cancer. He points out that besides being a methyl donor,
choline function as a "key component in the 'cellular
switchboard' that regulates the chemical signaling system in the
membranes of our cells." It is desirable to take folic acid
concurrently with choline; it seems that if more folic acid is
available, less choline is used up for methylation, and can thus be
used by the nervous system. Thus, methylating agents have a
choline-sparing action. Particularly as we grow older and our
absorption and the uptake of choline by the nervous system are likely
to decline, we simply can't afford to "waste" choline on
methylation while our cell membranes deteriorate.
A statement
in Dr. Craig Cooney's book, Methyl Magic, suggests that taking your
choline supplement with coffee may increase the release of
acetylcholine. "Research with rats shows that a combination of
caffeine and choline releases much more acetylcholine than choline
alone," Cooney states. This is probably due to the fact that
caffeine competes with adenosine, an inhibitor of acetylcholine
synthesis.
Protection
against high cholesterol
Choline is also
an enormously important nutrient because it helps prevent the buildup
of cholesterol. It synergizes with inositol in its function as a
lipotropic-a compound that emulsifies fat, keeping it in liquid
suspension. As long as cholesterol is emulsified, it is not likely to
settle on artery walls or in the gallbladder. In addition,
phosphatidyl choline actually helps transport cholesterol and fats so
they can be used by the body, or else excreted. If you are watching
your cholesterol, you may also be engaging in a serious exercise
program. But beware: strenuous exercise such as marathon running may
seriously lower the levels of choline. A study of the Boston marathon
runners found as much as a 40% decrease in some runners. The reason
for this might be the need for choline in the metabolism of fats,
which is increased during exercise.
Fetal
development
Several
fascinating recent studies found that when pregnant rats were
supplemented with choline (four to seven times the amount present in
the standard rat chow) during the last half of pregnancy, their
offspring showed lifelong improved learning capacity, attentiveness
and memory. Furthermore, the rats born to choline supplemented
mothers did not show the decline in memory with aging that was
apparent in control rats. The extra choline during fetal development
apparently produced a more efficient nervous system and ensured
superior brain health for the rest of the animals' lives. Thus, there
is reason to think that prenatal choline supplementation results in
enhanced attention, faster and more persistent learning, and improved
cognitive function in general across the life span. If these exciting
findings apply to humans as well, the implications of prenatal
choline supplementation for human cognitive performance and continued
brain health in old age are staggering. Newborns continue to require
large amounts of choline for development. Normally choline is
supplied in mother's milk. However, it is worth repeating that the
amount of choline in breast milk correlates with dietary consumption
of choline. A nursing mother who doesn't consume choline- rich foods
runs the risk of depriving her child of the higher choline levels
that would ensure optimal brain development, and also of becoming
choline-deficient herself.
How much do you need?
It has been
suggested that especially the elderly should supplement with 1-3 g of
choline a day, along with methylating agents such as vitamins B12, B6
and folic acid. Dr. Cooney suggests increasing one's choline
supplementation as one gets older. While 250 mg might be sufficient
for a young person (though possibly not for a pregnant or nursing
woman), as we get older we should move to 500 mg, then 750 mg, until
we reach 1500 to 3000 mg a day in old age.
It appears that
supplementation with choline may increase acetylcholine synthesis by
promoting increased neuronal activity. Otherwise, the extra choline
is probably used for other purposes, mainly the crucial task of
building and maintaining brain cell membranes. Choline
supplementation has also been shown to increase the density of
certain cholinergic receptors.
Do note: if you
have never taken choline supplements before, do not start with a
large dose, particularly if you are still relatively young. To do so
might make you feel hyperactive or anxious. It is best to increase
your intake gradually, Dr. Cooney suggests. It is also recommended
that you concurrently take other methylating agents, such as folic
acid. Dr. Cooney states that the fishy smell sometimes associated
with ingestion of large doses of choline disappears if you take 800
mcg of folic acid with your choline.
Where to get
it
Stroke victims
have shown improvement when supplementing with
glyceryl-phosphorylcholine. In rat studies, tissue examination showed
that the administration of glyceryl-phosphorylcholine was able to
help repair damaged neurons. A large dose of
glyceryl-phosphorylcholine was also found to help prevent a
drug-induced drop in acetylcholine levels. Clinical trials with
glyceryl-phosphorylcholine in Alzheimer's patients showed that 1200
mg/day of glyceryl-phosphorylcholine produced a greater improvement
on most cognitive and behavioral measures than 1500 mg/day of
acetyl-l-carnitine. Glyceryl-phosphorylcholine has also been compared
with CDP-choline (cytidine diphosphocholine), and has been found to
produce superior results in patients with vascular dementia. Another
study found much higher plasma choline levels after injections of
glyceryl-phosphorylcholine than CDP-choline.
Glyceryl-phosphorylcholine appears to be the best choline donor in
the brain. Studies using glyceryl-phosphorylcholine as a choline
donor found typical multiple benefits. Besides the expected
improvements in memory and learning in older animals,
glyceryl-phosphorylcholine prevented the age-related loss of certain
cholinergic receptors, as well as the age-related loss of neural
tissue in the cerebellum. A combined administration of growth
hormone-releasing hormone (GHRH) and glyceryl-phosphorylcholine
produced a greater release of growth hormone than GHRH alone. The
potentiating effect of glyceryl-phosphorylcholine on growth hormone
release was more pronounced in older subjects. It is interesting to
note that a quart of cow milk contains about 250 mg of
glyceryl-phosphorylcholine and 50 mg of phosphatidyl-ethanolamine.
Since newborn mammals have a tremendous need for choline, it is not
surprising that milk should contain compounds that are the most
efficient choline donors. In order for oral
glyceryl-phosphorylcholine to increase the levels of acetylcholine,
several other co-factors are involved such as pantothenic acid
(vitamin B5) and methylation-enhancing nutrients such as folic acid,
B12 and TMG.
Maintaining
brain cell membrane integrity
Phosphatidylethanolamine
is part of the cell membrane, together with compounds such as
phosphatidyl choline, phosphatidyl inositol and phosphatidyl serine.
The individual properties of these various phospholipids and their
metabolites are now under intense investigation. We know that
phosphatidyl- ethanolamine is deficient in the neurons of the victims
of Alzheimer's disease. These patients are also deficient in other
phospholipids. But one need not be diagnosed with a degenerative
brain disorder in order to become gradually deficient in
phospholipids, including phosphatidyl- ethanolamine. The aging
process decreases the levels of phospholipids in cell membranes
throughout the body, with particularly disastrous consequences for
the brain. Because of the brain's enormous need for choline, some
phosphatidylethanolamine in neural membranes may be methylated as
needed to provide choline.
Dietary Sources
It is estimated
that the average American consumes 500 - 1000 mg of choline from
food. Health-conscious people, however, are likely to avoid the
richest sources of choline, such as eggs, meat and organ meats. If
you are interested in increasing your intake of choline from the
diet, let us suggest that you substantially increase your consumption
of fish. Fish is correctly known as "brain food," since it
supplies a lot of choline (fish lecithin is a particularly rich
source of choline) and nucleic acids, which provide building blocks
for the synthesis of new cells. Cold-water fish is also the richest
source of the much-needed omega-3 fatty acids, with their
anti-inflammatory and antidepressant properties. If you are
interested in protecting your brain function from the ravages of
aging, daily consumption of fish is one of the best dietary changes
you can make. Note that the fish-eating Japanese have an enviably low
incidence of Alzheimer's disease in spite of enjoying the longest
life expectancy in the world. This argues against the mainstream
belief that simply living long enough inevitably leads to Alzheimer's
disease. An adequate supply of choline, combined with
anti-inflammatory nutrients such as omega-3 fatty acids, may
significantly lower the risk of developing this tragic degenerative
disorder.
Increasing
neurotransmitter receptors
Phosphatidylserine
(PS) is a phospholipid that is part of every cell membrane in the
body. It is especially abundant in brain cells. One special function
of phosphatidylserine is to keep neuronal membranes flexible.
Adequate PS levels in cell membranes also enables the free flow of
nutrients into the cells and facilitates the removal of metabolic
waste products. Improved membrane function also means improved energy
production. Furthermore, PS facilitates the release of
neurotransmitters, including acetylcholine and dopamine. Thus, PS is
vital for neuronal communication. It has been shown that PS can
increase the number of neurotransmitter receptors back to youthful
levels. In one mouse study, supplementation with PS was found to
increase the density of NMDA receptors in the forebrain by 25%. PS
also increased the binding of glutamate and glycine to the NMDA
receptors. This improvement in receptor density and function
naturally leads to improved neural communication as the neural signal
gets stronger and can be transmitted with greater speed. This in turn
results in improved cognitive function, as shown by better memory and
learning, the typical outcome of studies on PS. In the most famous
human study, the researchers gave 300 mg of PS a day for 12 weeks to
149 subjects over 50. Various memory and learning tests were
administered before and after. The results showed that PS managed to
raise cognitive performance to the levels typical for as much as 12
years younger. In other words, it is possible that supplementation
with PS may be able to reverse over a decade's worth of cognitive
decline. The most dramatic improvement was seen in subjects with the
greatest degree of initial memory impairment. In addition, in one
study, aged animals supplemented with PS actually performed better
than young animals. A fascinating study found that Parkinson's
patients with a slowed EEG showed accelerated EEG in response to PS.
These dramatic results are probably due to better function of neural
membranes, increased density of neurostransmitter receptors, and
higher levels of acetylcholine and dopamine, as well as to enhanced
glucose metabolism. Holistic clinicians such as Dr. Khalsa are
thrilled with the improvements they see in older patients who start
taking PS: better memory, more mental alertness and clarity, more
energy and zest, a brighter mood.
Sources of glyceryl-
phosphorylcholine
Milk contains free
glyceryl-phosphorylcholine and glycerophosphoryl ethanolamine, which
also acts as a choline donor, since it can be methylated to
glyceryl-phosphorylcholine. Other choline-rich foods, such as
lecithin, provide bound forms of glyceryl-phosphorylcholine and
glycerophosphoryl-ethanolamine that are not readily utilized by the
body. Lecithin is about 8% glyceryl-phosphorylcholine and
glycerophosphoryl ethanolamine. Pure glyceryl-phosphorylcholine
powder, on the other hand, is very stable (no fatty acids) and
water-soluble. It is a much more efficient donor of choline than
lecithin. At present, glyceryl-phosphorylcholine is manufactured by
an Italian firm that uses a special patented process to extract it
from soybean lecithin. It is sold as a drug in Europe to treat
various forms of senility. For the first time,
glyceryl-phosphorylcholine is being offered in the United States as a
dietary supplement.
Another study
showed that supplementation with PS increased the beneficial alpha
brain waves by up to 20%. Interestingly, there is a decline in the
alpha-range brain waves as we age; PS may be able to prevent this
senescent pattern. By enhancing the release of neurotransmitters and
the number of receptors, improving energy production, and keeping
neural cell membranes flexible, PS helps the brain preserve youthful
levels of functioning. One of the most important anti-aging
supplements, PS optimizes neural communication and helps prevent
cortisol-related brain damage. Together with other nutrients that
improve neural membrane fluidity, and thus the efficiency of
neurotransmitter receptors, PS also appears to be an effective
antidepressant. Finally, phosphatidyl serine treatment has been shown
to produce significant clinical improvement in early stages of
dementia. Doses as large as 300 - 500 mg may be needed.
Phosphatidyl
serine is widely present in foods, but only in trace amounts. It is
not possible to obtain enough PS from the diet; the body has to
synthesize it, and apparently does it less and less efficiently as we
age. Fortunately, the effectiveness of PS supplementation has been
widely documented. Please note: if you take phosphatidylserine (PS)
supplements, you should also take antioxidants to protect PS from
free radicals.
A critical cofactor needed to produce
acetylcholine
Pantothenic acid, also known as vitamin B5,
is a little-publicized key nutrient for neuroprotection. Pantothenic
acid is converted in our bodies into pantethine, which in turn serves
as a substrate for the synthesis of Coenzyme A (CoA). CoA improves
brain function by promoting the synthesis of acetylcholine.
Metabolites of CoA enhance brain metabolism and energy production
through its essential role in the Krebs cycle. The more energy brain
cells have, the better they can function in signal transmission, as
well as repair themselves and defend against free radicals. Another
indirect contribution of pantothenic acid to brain health stems from
the fact that CoA improves the metabolism of the heart muscle and
lowers serum lipids, thus improving blood flow to the brain. Yet
another benefit of pantothenic acid is the increased formation of
acetylcholine in the intestines. This intestinal acetylcholine
enhances peristalsis (rhythmic intestinal motion), thus preventing
constipation and facilitating elimination. Faster peristalsis also
means less complete digestion of food, helping prevent obesity.
An increased
susceptibility to infections, fatigue and decreased ability to cope
with stress could indicate a deficiency of pantothenic acid. This
important B vitamin has been shown to help in wound healing,
arthritis, building immune antibodies and lowering the toxicity of
many antibiotics. Like many other cardioprotective and
energy-enhancing compounds, pantothenic acid also appears to protect
against cancer. It even helps remove lipofuscin, the ugly brown
pigment in "age spots." More importantly, though, is the
fact that the brain uses pantothenic acid to transform choline into
acetylcholine.
"Viagra"
for the brain
First introduced 22 years ago in Hungary for
the treatment of vascular dementia-a disorder resulting from
insufficient blood flow to the brain tissue-vinpocetine has gradually
gained popularity as a European "smart drug." Recently it
has become available in the United States. It is a promising
neuroprotective supplement and cognitive booster. It is interesting
that vinpocetine has a similar mechanism of action as Viagra. Both
are known to be effective phosphodiesterase inhibitors. That is, they
work to enhance blood flow by inhibiting an enzyme in the
phosphodiesterase family. Not surprisingly, the main benefit of
vinpocetine is an improvement in cerebral blood flow. More blood
reaching the brain cells means better oxygenation, nutrition and
waste removal-all of which adds up to more youthful brain function.
Vinpocetine
has also been found to improve the transport of glucose (both uptake
and release) across the blood-brain barrier. Low cellular energy
production is perhaps the primary factor underlying all aging-related
brain degeneration. In addition, vinpocetine has been shown to
increase the firing rate of certain types of noradrenergic neurons,
which could explain one mechanism of its action as a cognitive
booster. The enhancement of blood flow and energy production means
that vinpocetine is particularly recommended for people whose
cognitive dysfunction stems chiefly from insufficient blood flow to
the brain. Vinpocetine also shows promise in helping prevent damage
to vision, especially dry macular degeneration. Vinpocetine likewise
appears to improve blood flow to the inner ear, thus protecting
hearing. Interestingly, vinpocetine has likewise been found to
counteract space motion sickness. It can also partly protect against
the damage resulting from excess glutamate and other excitotoxins. A
new neuroprotective property of vinpocetine has just been discovered:
it can lower the production of inflammatory cytokines. Together with
other phosphodiesterase inhibitors, vinpocetine has been shown to
lower the production by the microglia of a major inflammatory
compound known as tumor necrosis factor-alpha (TNF-alpha). Some
alternative clinicians believe that if we could truly control
inflammation, we could prevent Alzheimer's disease. This view is
based on the proven effectiveness of anti-inflammatories such as
ibuprofen in lowering the risk of Alzheimer's disease. The problem
with commonly used pharmaceutical anti-inflammatories is their side
effects. Vinpocetine and other natural anti-inflammatories (fish oil,
vitamin E, estrogens, many antioxidants including bilberry extract
and green tea catechins) appear to be a nontoxic alternative.
Vinpocetine is an alkaloid, in the same family as caffeine and
nicotine, both known to be very effective cognitive enhancers.
Nicotine increases the release of acetylcholine and dopamine, and
improves both short-term recall and long-term potentiation. But while
caffeine and nicotine each have well-known drawbacks, vinpocetine
appears to be safe and non-addictive. It would not be surprising if
vinpocetine shared nicotine's protective benefits against Alzheimer's
disease and Parkinson's disease, without the problem of addiction. An
interesting side benefit of vinpocetine is that it has also been
found to protect against both gastric and cerebral damage induced by
alcohol, against kidney problems caused by renal vasoconstriction,
and against retinal damage caused by the hepatitis B virus.
Enhancing Short-Term Memory
Another natural
memory enhancer, Huperzine A-an extract from the Chinese club
moss-appears to maintain higher acetylcholine levels by inhibiting
acetylcholinesterase, the enzyme that breaks down acetylcholine.
While it appears to be a promising adjuvant agent in the treatment of
Alzheimer's disease, it is still too early to say whether it is
desirable for people who have only minor memory deficit. Huperzine A
is a great short-term memory booster that can be taken in doses of 50
mcg to 100 mcg first thing in the morning for special situations
where maximum cognitive function is required. While Huperzine A
appears to be safe for special situations, daily use could cause a
neurotransmitter imbalance that could lead to undesirable
complications such as acetylcholine overload. Huperzine A should not
be taken more than a few times a week at the most.
Hormone
of memory and good cheer
Pregnenolone was discovered
during the 1930s and was extensively studied at first, particularly
in connection with job performance and as a therapy for arthritis.
Then it faded into oblivion as other hormones, notably synthetic
forms of cortisone, became more trendy, not to mention lucrative for
the drug industry. Now we are witnessing a revival of interest in
pregnenolone-after 60 years, it's gaining popularity alongside DHEA.
Pregnenolone functions largely as a pro-hormone. Produced primarily
in the adrenals, it is also the primary precursor of all the steroid
hormones, the first hormone to be formed from cholesterol, the raw
material for all steroids. The levels of pregnenolone go down with
aging. By the time we are 75, we have only 40% of the pregnenolone we
had when we were 35. Besides aging, stress, disease, hypothyroidism,
exposure to toxins and depression all result in low pregnenolone
levels. Patients suffering from depression have been found to have
pregnenolone levels less than half those found in nondepressed
persons. These decreased levels of pregnenolone have been found in
both unipolar and bipolar depression (the manic-depressive disorder).
In job-performance studies, subjects reported better mood when taking
pregnenolone. Like estrogen and DHEA, pregnenolone seems to have a
pleasantly stimulatory effect on the brain, making one feel sharp
without that wired, jittery feeling that may come from too much
caffeine, for instance. While many people know that DHEA and its
sulfate, DHEA-S, are very abundant in the brain, few know that the
brain levels of pregnenolone and pregnenolone sulfate are 10 times as
high as those of DHEA. Pregnenolone could be called our primary
neurosteroid. It is produced not only in the adrenals, but also in
the brain-a finding first reported by the famous French steroid
researcher, Dr. Etienne-Emile Baulieu. The peripheral nervous system
can also manufacture pregnenolone, possibly for the purpose of
maintaining the myelin sheath. Pregnenolone is somewhat like ginseng.
It improves energy, endurance and ability to cope with stress.
Studies using factory workers, college students and airline pilots
all found that pregnenolone effectively counteracts fatigue. When you
are under stress, pregnenolone gives you an extra edge. When you are
relaxed, however, you tend not to feel much difference. This may be
particularly true of younger people. The elderly, who are more
seriously deficient, seem to appreciate pregnenolone's extra energy
boost more keenly. In the 1940s, it was established that pregnenolone
facilitates learning and helps us perform any task in which memory is
involved. But pregnenolone's chief claim to fame is the fact that
this pre-hormone has been found to be the most effective memory
booster yet discovered in animal studies. It has been shown to
increase the release of acetylcholine and to modulate NMDA
(aspartate/glutamate) receptors in a way that suggests that
pregnenolone stimulates central cholinergic communication. It also
seems to modulate enzyme activity, calcium-ion flow through cell
membranes, protein turnover and other complex reactions involved in
memory function. Together with DHEA, pregnenolone also synchronizes
the firing of the neurons. A decline in pregnenolone thus makes all
mental function more difficult. There is some anecdotal evidence
suggesting that pregnenolone may be especially effective in elderly
women as a restorer of energy and mental clarity, and as an
antidepressant. Even a small amount of supplemental pregnenolone may
affect the quality of sleep. Most studies find that pregnenolone,
like DHEA, increases the amount of REM sleep, which appears to be
play a role in the formation of memory. Like progesterone,
pregnenolone is also important for repairing the brain and the spinal
cord in case of injury. Pregnenolone is a precursor to progesterone
in the body. Caution: Men diagnosed with prostate cancer are advised
to avoid pregnenolone because of the possibility of conversion into
androgens.
Brain
boosters
There are a
variety of other supplements that may enhance your brain longevity
program. Among these is alpha lipoic acid, which is both an
antioxidant and a metabolic enhancer and has emerged as a new star.
It is joined by neuroprotective energy-enhancers: acetyl-L-carnitine
and coQ10. The nervous system also needs the benefits of antioxidants
and anti-inflammatories such as vitamin E, shown not only to protect
the membranes but also to restore damaged neurotransmitter receptors,
and fish oil. After all, fish eating has been documented to correlate
with a dramatic lower risk of Alzheimer's disease. Neuroprotective
regimens should also include the catechins in green tea extract,
and/or the proanthocyanidins in grape seed extract and similar
compounds in bilberry extract. High-potency ginkgo is also highly
recommended. In addition to being a documented cognitive enhancer, it
has recently been found to extend life span in rats. Improvement in
Alzheimer's disease patients has been noted with doses of 240 mg and
higher.
Getting enough
sleep and rest is extremely important. We must also take measures to
reduce cortisol, which has neurotoxic effects. Meditation and stress
reduction are effective measures, as are supplements such as DHEA,
pregnenolone, and KH3. Chronic stress, today the daily condition of
millions, causes an increase in free radicals (both oxygen and nitric
oxide-based) and inflammatory cytokines. Fortunately most of the
compounds mentioned here are both excellent antioxidants and
anti-inflammatories; vitamin E and green tea catechins are stellar
examples. Finally, vitamin C is extremely important for the brain.
Besides functioning as an antioxidant, it also enhances the synthesis
of key neurotransmitters, including acetylcholine and dopamine.
Niacin (B3) also helps manufacture neurotransmitters, including the
calming GABA. Interestingly, yet another B vitamin, thiamin (vitamin
B1) has turned out to be a potent antioxidant, helping other
antioxidants such as vitamin E to destroy free radicals.
Conclusion
Remember: unless
you slow down your aging, aging is going to slow you down. It will
make you increasingly physically and mentally disabled, sluggish,
forgetful and depressed, ultimately making life not seem worth
living. Fortunately, you can fight back with lifestyle, the right
diet and the right supplements.
References
Aleppo G et al.
Chronic glyceryl-phosphorylcholine increases inositol phosphate
formation in brain slices and neuronal cultures. Pharmacol Toxicol
1994; 74:95-100.
Amenta F et al. Cholinergic neurotransmission
in the hippocampus of aged rats: influence of
glyceryl-phosphorylcholine treatment. Ann NY Acad Sci 1993:
695:311-3.
Borghese CM et al. Phosphatidyl serine increases
hippocampal synaptic efficacy. Brain Res 1993; 31:697-700.
Bronzetti
E et al. Effects of ipsilateral lesioning of the nucleus basalis
magnocellularis and of glyceryl-phosphorylcholine treatment on
acetyltransferase and acetylcholinesterase in the rat front-parietal
cortex. Neurosci Lett 1993; 164:47-50.
Ceda CP et al.
Glyceryl-phosphorylcholine administration increases the growth
hormone responses to GHRH of young and elderly subjects. Horm
Metabolism Res 1992; 24:119-21.
Ceda GP et al.
Glyceryl-phosphorylcholine administration increases the growth
hormone response to GHRH in young and elderly subjects. Horm
Metabolism Res 1992; 24: 119-21.
Cermak JM et al. Prenatal
availability of choline alters the development of
acetylcholinesterase in the rat hippocampus. Dev Neurosci 1999;
21:94-104.
Chalimoniuk M, Strosznaider JB. Aging modulates
nitric oxide synthesis and cGMP levels in hippocampus and cerebellum.
Mol Chem Neuropathol 1998; 35:77-95.
Coccoli C.
Glyceryl-phosphorylcholine and glycerophosphorylethanolamine: their
preparation and uses (Manufacturer's pamphlet)
Cohen SA et al.
Age-related alteration in NMDA-receptor properties in the mouse
forebrain: partial restoration by phosphatidyl serine treatment.
Brain Res 1992; 584:174-80.
Cooney C and Lawren B. Methyl
Magic. Andrews McMeel Publishing, 1999; quotation about choline and
membrane chemical signaling, p. 132.
Coutcher JB et al.
Dietary choline supplementation increases the density of nicotine
binding sites in rat brain. J Pharmacol Exp Ther 1992;
262:1128-32.
Crook T et al. Effects of phosphatidyl serine in
age-associated memory impairment. Neurology 1991; 4:644-9.
Crook
T et al. Effects of phosphatidyl serine in Alzheimer's disease.
Psychopharmacol Bull 1992; 28:61-66.
Di Perri R et al. A
multicentre trial to evaluate the efficacy and tolerability of
glyceryl-phosphorylcholine versus cytosine diphosphocholine in
patients with vascular dementia. J Int Med Res 1991; 19:330-41
Dolby
V. Pregnenolone. Keats Publishing, 1998.
Fallbrook A et al.
Phosphatidyl choline and phosphatidyl ethanolamine metabolites may
regulate brain phospholipid catabolism via inhibition of
lysophospholipase activity. Brain Res 1999; 834:207-10.
Flood
JF et al. Memory-enhancing effects in male mice of pregnenolone and
steroids metabolically derived from it. Proc Natl Acad Sci USA 1992;
89:1567-71.
Fujii S et al. Acute and chronic nicotine exposure
differentially facilitate the induction of LTP.Brain Res 1999;
846:137-143.
Funfgeld EW et al. Double-blind study with
phosphatidyl serine in Parkinsonian patients with senile dementia of
Alzheimer's type. Progesterone Clin Biol Res 1989;
317:1235-46.
Gatti G et al. A comparative study of free plasma
choline levels following intramuscular administration of
glyceryl-phosphorylcholine and citicoline in normal volunteers. Int J
Clin Pharmacol Ther Toxicol 1992; 30:331-5.
Gimenez R et al.
Cytidine diphosphate choline administration activates brain cytidine
triphosphate: phosphocholine cytidylytransferase in aged rats.
Neurosci Lett 1999; 273:163-6.
Gulyas B et al. Cerebral uptake
and metabolism of vinpocetine in monkeys: PET studies. Orv Hetil
1999;140:1687-91.
Hogervorst E et al. Caffeine improves
cognitive performance after strenuous physical exercise. Int J Sports
Med 1999; 20:354-61.
Jacob RA et al. Folate nutriture alters
choline status of women and men fed low choline diets. J Nutr 1999;
129:712-7.
Khalsa DS. Brain Longevity. Warner Books,
1997.
Kidd PM. A review of nutrients and botanicals in the
integrative management of cognitive dysfunction. Altern Med Rev 1999;
4:144-61.
Koyama Y et al. How does the distension of urinary
bladder cause arousal? Psychiatry Clin Neurosci 1998;
52:142-5.
Lillestl IK et al. Relaxing effects of cyclic GMP
and cyclic AMP-enhancing agents on the long-lasting contraction to
endothelin-1 in the porcine coronary artery. Scand J Clin Lab Invest
1998; 58:625-34.
Martinez M, Mougan I. Fatty acid composition
of human brain phospholipids during normal development. J Neurochem
1998; 71:2528-33.
Meck WH et al. Organizational changes in
cholinergic activity and enhanced visuospatial memory as a function
of choline administered prenatally or postnatally or both. Behav
Neurosci 1989; 103:1234-41.
Meier-Ruge WA, Bertoni-Freddari C.
Mitochondrial genome lesions in the pathogenesis of sporadic
Alzheimer's disease. Gerontology 1999; 45:289-97.
Molnar P et
al. The impairment of long-term potentiation in rats with medial
septal lesion and its restoration by cognitive enhancers.
Neurobiology 1994; 2:225-66.
Monteleone P et
al. Blunting by chronic phosphatidyl serine administration of the
stress-induced activation of the hypothalamo-pituitary-adrenal axis
in healthy men. Eur J Clin Pharmacol 1992; 42:385-8.
"Over
75 mental decline steeper than expected." Reuters Health,
November 3, 1999.
Packer L and Colman C. The Antioxidant
Miracle. John Wiley and Son, 1999.
Pallares M et al. The
neurosteroid pregnenolone sulfate infused into the nucleus basalis
increases both acetylcholine release in the frontal cortex or
amygdala and spatial memory. Neuroscience 1998; 87:551-8.
Pan
Y et al. Effect of estradiol and soy phytoestrogens on choline
acetyltransferase and nerve growth factor mRNAs in the frontal cortex
and hippocampus of female rats. Proc Soc Exp Biol Med 1999;
221:118-25.
Parnetti L et al. Multicentre study of
l-alpha-glyceryl-phosphorylcholine vs ST200 among patients with
probable senile dementia of Alzheimer's type. Drugs & Aging,
1993; 3:159-64.
Pyapali GK et al. Prenatal dietary choline
supplementation decreases the threshold for induction of long-term
potentiation in young adult rats. J Neurophysiol 1998;
79:1790-96.
Regelson W, Colman C. The Superhormone Promise.
Simon and Schuster, 1996.
Sangiorgi GB et al.
Glyceryl-phosphorylcholine in the mental recovery of cerebral
ischemic attacks. Ann NY Acad Sci 1994; 717:253-69.
Schettini
G et al. Molecular mechanisms for mediating the effects of
glyceryl-phosphorylcholine, a new cognition-enhancing drug, on
behavioral and biochemical parameters in young and aged rats.
Pharmacol Biochem Behav 1992; 43:139-51.
Sicurella L et al.
Evoked visual potentials modifications in subjects treated with
glyceryl-phosphorylcholine. Manufacturer's Pamphlet.
Szakall S
et al. Cerebral effects of a single dose of intravenous vinpocetine
in chronic stroke patients: a PET study. J Neuroimaging 1998;
8:197-204.
Szutowicz A et al. Key role of acetyl-CoA in
cytoplasm of nerve terminals in disturbances of acetylcholine
metabolism in the brain. Folia Neuropathol 1997; 35:241-3.
Vallee
M et al. Neurosteroids: deficient cognitive performance in aged rats
depends on low pregnenolone sulfate levels in the hippocampus. Proc
Natl Acad Sci USA 1997; 94:14865-70.
Warburton DM. Effects of
caffeine on cognition and mood without caffeine abstinence.
Psychopharmacology 1995; 119:66-70.
Wecker L. Influence of
dietary choline availability and neuronal demand on acetylcholine
synthesis by rat brain. J Neurochem 1988; 51:497-504.
Wecker
L. Neurochemical effects of choline supplementation. Can J Physiol
Pharmacol 1986; 64:329-33.
Weinman B et al. Studies on wound
healing: effects of calcium D-pantothenate on the migration,
proliferation and protein synthesis of human dermal fibroblasts in
culture. Internat J Vitamin Nutr Res 1999; 69:113-19.
Yoshikawa
M et al. Effects of phosphodiesterase inhibitors on cytokine
production by microglia. Mult Scler 1999; 5:126-33.
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