A mind is a terrible thing to waste. This is your brain on drugs. Based on
classic advertising slogans, America has historically mistreated its primary
operating system. While there certainly are aspects of modern lifestyles that
tax the brain and cause people to lose their minds, many have found dietary and
nutritional tools can help strengthen the brain against degeneration from aging
and abuse.
Of all the body’s parts and systems, the brain represents the most of who a
person is—it’s the base of personality, emotion, reasoning and memory, and
it controls movements and every body function. This 2- to 3-pound blob of tissue
houses an average 100 billion neurons and at least 10 times as many glial
cells—non-neuronal cells that provide nutrition, contribute to signal
transmission and form phospholipid myelin sheaths, which surround nerve fibers.
It is the base of the central nervous system, and is comprised of 79-percent
water, 10-percent lipids, 8-percent protein and 1-percent carbohydrate. As with
any major organ, nutrients are crucial to survival and performance.
The integrity of the brain, its structure and function, factors heavily in
cognitive performance. There are numerous threats to neurons, nerves, neuronal
signaling and neurotransmitters that aid these signals. As a lipid-rich tissue,
the brain is especially susceptible to oxidation, which increases with age and
is menacing to neuronal tissue. As is the case in the rest of the body,
oxidation can damage cells, tissues and genetic material in the brain. Research
has demonstrated cellular generation of reactive oxygen species (ROS) causes
oxidative damage to nucleic acid, carbohydrate, protein and lipid components of
the brain, where damaged neuronal cells—which are primarily not
regenerative—cannot be replaced readily via mitosis (cell duplication).1
Unchecked oxidation can sap performance and contribute to degenerative illnesses
such as Alzheimer’s disease (AD), amyotrophic lateral sclerosis (ALS, Lou
Gehrig’s disease) and dementia. In fact, oxidation from broken-down beta
amyloid plaques causes normally helpful immune macrophage cells in the brain to
produce toxic cytokines, such as interleukin-6 (IL-6), seen in high amounts in
AD patients.
In the brain, a number of antioxidant nutrients shine. Italian researchers
drew a connection between AD and mi ld cognitive impairment, and depressed
peripheral levels of antioxidants, including vitamins A, C and E, carotenoids
(lutein, zeaxanthin, beta-cryptoxanthin, lycopene, alphacarotene and
beta-carotene) and superoxide dismutase (SOD).2
More recently, French scientists used a cross - sectional analysis to compare
plasma levels of those same carotenoids with performance on a range of cognitive
tests in a population of more than 1,300 healthy, elderly people. Participants
in the lowest quartile of cognitive function had a higher probability of having
low levels of lycopene and zeaxanthin.3
Similarly, University of Washington researchers monitored long-term
antioxidant status and cognitive function in a seven-year study of 2,082
community-dwelling elderly subjects, finding those who supplemented with
vitamins A, C or E, plus selenium or zinc, had a 34-percent lower risk of
developing cognitive impairment and a 29-percent lower risk of experiencing
cognitive decline, compared with nonantioxidant users.4
The
powerful antioxidant coenzyme Q10 (CoQ10) is an important component of the
electron transport chain and, thus, addresses free radicals produced during
oxidative phosphorylation in the inner mitochondrial membrane.5 CoQ10
can be manufactured in the body, but levels decline due to aging; scientists
have found replenishing these levels via CoQ10 supplementation may help stave
off AD, Parkinson’s disease (PD) and other neurodegenerative disorders.6
In 2005, University of Coimbra, Portugal, researchers discovered CoQ10 treatment
in aged, diabetic rats counteracted brain mitochondrial alterations induced by
Abeta1-40 amyloid peptide, suggesting, “CoQ10 therapy can help to avoid a
drastic energy deficiency that characterizes diabetes and Alzheimer’s disease
pathophysiology.”7 Subsequent studies out of Hong Kong confirmed
CoQ10 supplementation protects neuronal cells from amyloid peptide toxicity by
reducing the concentration of superoxideanion.8 Combined
supplementation with CoQ10 and alpha-tocopherols in aged mice improved brain
function, as measured by cognitive tests, according to research from the
University of North Texas, Fort Worth.9
Another powerful antioxidant for brain function, alpha lipoic acid (ALA) is
both water- and fat-soluble and is capable of crossing the blood-brain barrier.
Research has shown ALA protects against the effects of oxidative damage on
electron transport and the mitochondria, which is especially prone to free
radicals.10 Clinical studies have shown ALA may help maintain healthy
memory and mental focus,11 and improve memory, especially in older
adults.12
Another threat to brain health is homocysteine, a relative of the amino acid
cysteine. Elevated levels of homocysteine have been linked to brain atrophy and
cerebrovascular disease, two key factors in the development and progression of
dementia and AD.13,14 High homocysteine levels have since been linked
to ischemic events, including stroke, as well as cardiovascular problems—blood
flow to the brain is important for nutrient delivery. Fortunately, B vitamins,
including B12, B6 and folic acid, have a good track record on lowering
homocysteine levels.15
Researchers from the University of Oxford, England, and University of Oslo,
Norway, recently analyzed data from the population-based Rotterdam Scan Study,
including 1,033 nondemented participants aged 60 to 90, who underwent extensive
cognitive testing and brain imaging.16 Test scores showed
improvements in global cognitive function, psychomotor speed and memory
function, relative to folate concentration increases. Researcher s suggested the
performance improvements may be regulated by vascular mechanisms.
Vascular problems endanger brain nutrition and function, especially on the
microvascular level. One herbal supplement indicated for improved cerebral
circulation is vinpocetine, a derivative of periwinkle (Vinca minor). Research
shows vinpocetine increases blood flow to the brain by reducing the flow
resistance of cerebral vessels;17 it also inhibits platelet
aggregation and increases the deformability of red blood cells of erythrocytes.18
Studies in humans and in animal models have found vinpocetine can increase
short-term memory and critical reaction time in healthy adults.19
According to Mel issa Wi lson, quality assurance coordinator at J.R. Carlson
Laboratories, vitamin E is another natural solution for maintaining healthy
blood vessels and other healthy tissues by promoting the healthy function of our
blood vessel linings and preventing oxidative damage. “One study20
concluded vitamin E intake, from foods or supplements, is associated with less
cognitive decline with age,” she said, adding in another recent study,
supplemental vitamins E and C were associated with cognitive benefits in elderly
women.21
However, the most well -known herbal remedy for improved vascular health,
especially in the brain, is Ginkgo biloba. A study from the Institute of
Microcirculation, Beijing, found ginkgo extract (EGb 761) increased blood
perfusion, regulated vasomotion function, opened capillaries and released the
peripheral resistance in the cerebral cortex of hypertensive rats.22
Due to its effects on blood flow and vascular health, as well as its
antioxidant properties, ginkgo has been touted for improved memory and cognitive
function. On cognition, Polish researchers found preventive doses of 100 mg/kg
ginkgo in rats prior to a two-hour episode of restraint stress or corticosterone
inject ion abolished cognitive deficits, as measured by decreased re-entry
latencies in a passive avoidance test.23 Subsequent study by the same
researchers revealed 100 mg/kg doses of EGb 761 improved spatial and nonspatial
memory in the Morris water maze and object recognition tests in chronically
stressed or corticosterone-treated rats.24 A pair of Chinese studies
also reported ginkgo had positive effects on spatial learning and memory.25,26
A Cochrane review concluded ginkgo has benefits on mood and cognitive
function at doses less than 2 0 0 mg/d for periods around 12 weeks.27 This
exact ginkgo extract is one of the keystone ingredients in Enzymatic Therapy’s
Remember!™ formulation. Cheryl Myers, vice president of health sciences at
Enzymatic Therapy, said in addition to including ginkgo in its recognized
standardization, the formula contains B vitamins for their role in reducing
homocysteine and Bacopa monnieri for its benefits to cognitive
performance and memory.
In 20 01, Australian scientists reported 300 mg/d of bacopa “may improve
higher order cognitive processes that are critically dependent on the input of
information from our environment such as learning and memory.”28
On memory, additional Australian research suggested bacopa decreases the rate
of forgetting of newly acquired information.29 Subsequent study has
confirmed bacosides from the herb support anterograde memory (forming new
memories) and control anterograde amnesia, insufficient transfer of new events
from short- to long-term memory.30
Inflammation, when not properly controlled or balanced, is another danger to
the brain. Italian scientists linked inflammation and inadequate antioxidant
defenses to accelerated decline of nerve conduction velocity over the aging
process.31 Tea catechins offer potent antioxidant and
anti-inflammatory activities, which are helpful in fighting age-associated
cognitive decline and neuronal loss in neurodegenerative conditions, such as AD,
PD and Huntington’s diseases;32 catechins also inhibit neuronal
death in a wide array of cellular and animal models of neurological disorders.33
In 2007, researchers from Ohio State University linked the known
anti-inflammatory actions of omega-3 fatty acid DHA (docosahexaenoic acid) with
neuroinflammation related to arachidonic acid derivatives.34 They
found DHA and its lipid mediators inhibit transcription factor NFkappaB, prevent
cytokine secretion, block the synthesis of prostaglandins, leukotrienes and
thromboxanes, and modulate leukocyte trafficking.
Omega-3 fatty acids have multiple actions in the brain. DHA has also shown an
ability to reduce amyloid beta levels, compared to a control diet, as well as
decrease the number of activated microglia (immune cells) in the hippocampus and
boost the exploratory activities of mice, although there was no effect on
spatial learning.35 Subsequent study of AD by University of
California, Irvine, scientists revealed DHA reduced soluble amyloid beta by
decreasing steady-state levels of presenilin 1 (AD gene).36
Supplementation with fish oil rich in DHA can not only support infant brain
development37 and promote higher IQ,38 but it also slows
memory decline in aging populations.39
Myers called fish oil her second top brain supplement—CoQ10 was number
one—but advised consumers to seek out a full-spectrum, high quality fish oil.
“Rancidity can generate one of the worst kinds of free radicals, hydroxyl
radical,” she said. “Why use a product for its benefits only to create
another problem?”
Transmission Failures
Neurotransmitters help neurons signal or communicate with other neurons
within the central nervous system. Acetylcholine, the first neurotransmitter
identified, is important to autonomic nerve signaling, especially in the brain,
where it affects memory, focus, concentration and muscle memory. Acetylcholine
is synthesized from choline, a lipid-bound essential nutrient. A rich source of
cholineis phosphatidylcholine (PC), a phospholipid found commonly in egg yolks,
soy and liver meat.
Alpha-glyceryl phosphoryl choline (A-GPC) is basically PC minus two fatty
acid chains. This phospholipid-derived compound has shown potential in
countering the loss of acetylcholine receptors in aging animals.40
Early in vitro work suggested A-GPC treatment may result in an increased rate of
phospholipid synthesis, including the phosphoinositides available for signal
transduction at central nervous system level.41
“A-GPC has been used in Europe and Asia as a nutrient to address a variety
of cognitive indications, including Alzheimer’s disease, and to optimize
neurological and muscle response in athletes,” said Scott Hagerman, president
and CEO of Chemi Nutra. “In fact, a recently published study on A-GPC showed
that it very, very effectively improved conditions associated with Alzheimer’s
disease.” This multicenter, double blind, randomized, placebo-controlled trial
involved 261 patients affected by mild to moderate dementia of the Alzheimer
type, who were treated with 400 mg A-GPC or placebo capsules three times daily
for 180 days.42 According to the researchers, the results of numerous
AD-cognitive tests suggested clinical usefulness and tolerability of A-GPC in
the treatment of the cognitive symptoms of dementia disorders related to AD.
Citicoline, an intermediate of structural phospholipids such as PC in the
brain, activates biosynthesis of structural phospholipids of neuronal membranes,
increases brain metabolism, and acts upon the levels of different
neurotransmitters, according to a Spanish review.43 They noted
citicoline is widely distributed throughout the body, crosses the blood-brain
barrier and reaches the central nervous system, where it is incorporated into
the membrane and microsomal phospholipid fraction. A 2004 Cochrane review noted
CDP-choline has a positive effect on memory and behavior in the short- to
medium-term.44 The use of citicoline has al so been as sociated with
improvement in some aspects of declarative memory, especially in cocaine
abusers.45
Among phospholid- related supplements for brain health, phosphatidylserine
(PS) has garnered increased attention for its critical role in slowing memory
loss and cognitive decline from severe neurological disorders. In 2007, Japanese
researchers reported pretreatment of microglia with PS/PC liposomes considerably
inhibited the TNF-alpha, NO and superoxide production induced by amyloid
beta/IFNgamma.46 They concluded PS/PC liposomes have both
neuroprotective and antioxidative properties through the inhibition of
microglial activation, thus suppor ting the memory/cognitive-enhancing and
anti-dementia effect of PS.
Hagerman noted Chemi Nutra’s SerinAid® PS was evaluated in a research
study at the University of Guadalajara, Mexico, involving PS and its ability to
reduce the incidence of memory loss that accompanies hormone replacement therapy
(HRT) in women.47 In the final report, the researcher commented that
PS “improved various emotional aspects related to HRT.”
Orly Farkash, head of marketing, Enzymotec, reported while the mechanism of
action for PS is still under investigation, scientists have noted its
involvement in the cholinergic system, as well as its role in maintaining normal
capacity for norepinephrine, serotonin and dopamine dependent neurotransmitter
systems that are essential for the normal functioning of the central nervous
system and transmission of nerve impulses across the body.
Michael Wilson, vice president, Vital Basics Inc., maker of Focus Factor,
said: “It is noteworthy there are two health claims approved in 2003 by FDA
for PS: Phosphatidylserine may reduce the risk of cognitive dysfunction in the
elderly; and Phosphatidylserine may reduce the risk of dementia in the
elderly.”
He further noted in a small, unpublished double blind, placebo-controlled
study in 2001, Focus Factor improved several aspects of memory and cognition in
middle-aged adults. Researchers noted subjects who took the supplement during a
two-week period experienced an overall improvement in cognitive function,
immediate and delayed memory, language, visuospatial/constructional memory, and
attention. Specifically, subjects in the treatment group improved in 10 of the
13 individual tests measuring immediate and delayed memory;
visuospatial/constructional memory and attention; and cognition and visuospatial
working memory.
Focus Factor contains a spectrum of vitamins, minerals, ant ioxidants,
omega-3 fatty acids (DHA), as wel l as “neuronutrients” such as PS,
vinpocetine and huperzine. Huper zine A (HupA), derived from Chinese club moss (Huperzia
serrata), offers neuroprotective effects.48 According to a review
from the Shanghai Institutes for Biological Sciences, HupA may protect cells
against hydrogen peroxide, betaamyloid protein, glutamate, ischemia and
staurosporineinduced cytotoxicity and apoptosis; has been found to reverse or
attenuate cognitive deficits in a broad range of animal models; and has
significantly attenuated memory deficits in aged human subjects as well as
patients with benign senescent forgetfulness, AD and vascular dementia (VD),
with minimal peripheral cholinergic side effects.49 Animal study
showed huperzine reduced memory impairment, reduced neuronal degeneration in the
CA1 region, and partially restored hippocampal choline acetyltransferase
activity;50 these results suggested HupA might at tenuate memory
deficits and neuronal damage after ischemia and might be beneficial in
cerebrovascular type dementia.
Mind over Matter
Healthy nerves, signaling, structures and memory formation are the nuts and
bolts of basic neurological function. Mood, mental wellness and stress relief
are enigmatic pysch-segments of brain health, but they more commonly affect
people of all demographics.
Some of the supplements researched for improved memory and cognitive function
are also indicated for improved mood or mental state. Hagerman noted PS is
becoming recognized as an effective alternative to invasive pharmaceutical
intervention for behavior modification such as in attention deficit disorder
(ADD) and attention deficit/hyperactive disorder (ADHD), as well as depression,
and mood disorders.
Similarly wide ranging, omega-3s from fish oil have been indicated in
managing mild to moderate depression. A 2007 meta-analysis of double blind,
placebo-controlled trials of antidepressant activity of omega-3 fatty acids from
fish oil found significant efficacy in treating depres s ion, though the author
s concede more large-scale trials are needed to confirm the findings.51
Depression and mood are linked to three primary hormones: serotonin,
norepineprhine and dopamine. However, depression can result from low serotonin
levels created by genetic disorder or the brain’s self-protect mechanism under
emotional stimuli. The go-to treatments for mild depression include: monoamine
oxidase (MAO) inhibitors, which protect monoamines such as serotonin and
dopamine from breakdown; tricyclics, which have a slew of undesirable side
effects; and selective serotonin reuptake inhibitors (SSRIs), which are
theorized to keep the serotonin in the synaptic gap longer.
St. John’s wort has been credited with numerous mechanisms of action
against depression, including SSRI and MAO inhibitor activities—but with fewer
side ef fects than pharmaceut ical equivalents. The focus has most recently been
on St. John’s wort as an SSRI.
The herb’s best results have come from studies showing efficacy against
mild or moderate depression.52,53 It has rout inel y compared
favorably to tricyclics and other standard antidepressants.54,55
However, it has had its share of critical research.56
“St. John’s wort works well for mild depression, but studies started
using it for more advanced, serious depression,” Myers said, adding these
ill-designed trials got widespread media coverage and helped dent the herb’s
rapidly growing popularity. “Also, because it helps speed up toxin removal in
the liver, St. John’s wort can interfere or shorten the life of a range of
pharmaceutical medications, so many people taking drugs for other problems have
shied away from St John’s wort.” Indeed, the herb has been contraindicated
with birth control, HIV meds and immune drugs.
The benefits of St. John’s wort have been increasingly linked to its
hypericin and hyper forin constituents, which increase hormones such as
dopamine, noradrenaline and GABA (gamma aminobutyric acid). GABA is a central
nervous system neurotransmitter that acts on certain brain synapses. Increased
levels of GABA can help defuse stress and ease anxiety. Decreased levels of GABA
have been linked to anxiety and panic at tack disorders,57,58 and
GABA agonists—bind to GABA receptors, thereby stimulating GABA-like
effects—have also been linked to improved sleep and relaxation.59,60
For example, Tahitian Noni International published research showing a noni
extract, specifically its ligands, has a propensity for binding with GABA-A
receptors as an agonist, inducing anxiolytic and sedative effects.61
Myers noted, “There is still a lot of scientific discovery going on with
GABA, so it is primarily bought by people who are up-to-date on the latest
research and like to be ahead of the curve on remedies .” She added another
supplement indicated for stress relief and improved mood is Holy Basil (Ocimum
sactum), an adaptogenic herb. She explained this type of herb does not alter
mood in ways other remedies do, but it helps the body adapt to stress by
maintaining healthy body functioning.
Holy basil contains many compounds that may be the root of its benefit in
stress. Test results published in 2007 highlight the various constituents in O.
sanctum and their effects on stress parameters, although the results did not
definitively pinpoint all the relevant compounds.62 Enzymatic
Therapy’s Holy Basil Trinity combines three different extracts—alcohol
(solvent), supercritical (CO2) and steam (H2O)—each which delivers a unique
roster of bas i l compounds. Myers said this represents the complete spectrum of
the beneficial compounds naturally found in the O. sanctum leaves.
Retailing Brain Science
Between cognitive function and memory boosters and mental wellness enhancers,
the brain health category is a viable market, if one hard to classify. “While
overall sales of dietary supplements reached $22 billion in 2006, it’s
difficult to quantify total sales specifically from cognitive function
supplements since many manufacturers choose not to reveal their figures (ABC
News cited a figure of $140 million in 2002),” Wilson noted. “But
demographic statistics paint a rosy picture for the future of brain-support
supplements.”
Farkash noted beyond category leaders ginkgo, omega- 3s and PS, there are no
other supplements well known in public for brain health or cognitive function.
“People are not aware enough that brain and mental capacity is prone to suffer
due to aging and that the process of cognitive deterioration could be slowed
down or even reversed back by supplementation,” she said. She added when
comparing the brain market (around $311 million) to that of heart health ($1.2
billion) or even joint health ($1.2 billion), it is clear that this market is
virtually under developed.
Hagerman agreed there is great potential in this market segment. “There has
been much written in the popular press about maintaining and improving memory,
primarily by exercising the mind through continued intellectual use and through
the use of mental exercises that help strengthen memory and concentration,” he
said. “In addition, research has shown support for a number of natural
ingredients, like phosphatidylserine (PS), A-GPC, acetyl-L-carnitine, ginkgo
biloba, and vinpocetine, among others, that have proven science to support their
use in enhancing mental performance under a variety of situations.”
Given the complexities of brain health and assortment of natural cognitive
and mental enhancers on the market, guiding customers to the right products for
the right problems is not a straight forward task. Robert Hunt, president of RZN
Nutraceuticals, explained restrictive FDA regulations present a challenge to
both manufacturers and retailers trying to introduce customers to brain health
alternatives. “It is important for manufacturers to offer viable alternatives
which have solid science and independent clinical research to support the claims
for products being offered,” he noted.
Myers confirmed this regulatory challenge, adding: “Because of the
limitations of structure-function statements, it can be hard for consumers to
differentiate between a row of different brain health products, each which can
often have a specific action or benefit. This is why it is important to have
staff educated on the different products, in order to help steer the consumer to
the most appropriate remedy.”
Hagerman stated, “The future for cognitive enhancing nutraceuticals remains
very bright and, every month, more innovative cognitive-improving natural
products are launched to receptive consumers who are acting proactively to their
mental, stress, and mood challenges.”
1. Lau FC et al. "The beneficial effects of fruit polyphenols on brain
aging." Neurobiol Aging. 26, Suppl 1:128-32, 2005. www.elsevier.com
2. Rinaldi P et al. "Plasma antioxidants are similarly depleted in mild
cognitive impairment and in Alzheimer's disease." Neurobiol Aging 24,
7:915-9, 2003. www.elsevier.com
3. Akbaraly NT et al. “Plasma carotenoid levels and cognitive performance
in an elderly population: results of the EVA Study.” J Gerentol Med Sci.
2007; 62A(3)308-16. http://biomed.gerontologyjournals.org
4. Gray SL et al. "Is antioxidant use protective of cognitive function
in the community-dwelling elderly?" Am J Geriatr Pharmacother. 1,
1:3-10, 2003.www.elsevier.com
6. Joseph JA, et al “Reversals of Age-Related Declines in Neuronal Signal
Transduction, Cognitive, and Motor Behavioral Deficits with Blueberry, Spinach,
or Strawberry Dietary Supplementation”, The Journal of Neuroscience,
19:8114-8121, 1999. http://www.jneurosci.org/cgi/reprint/19/18/8114.pdf
7. Moreira PI et al. “CoQ10 therapy attenuates amyloid beta-peptide
toxicity in brain mitochondria isolated from aged diabetic rats.” Exp
Neurol. 2005 Nov;196(1):112-9. http://dx.doi.org/10.1016/j.expneurol.2005.07.012
8. Li G. et al. “Coenzyme Q10 protects SHSY5Y neuronal cells from beta
amyloid toxicity and oxygen-glucose deprivation by inhibiting the opening of the
mitochondrial permeability transition pore.” Biofactors.
2005;25(1-4):97-107. http://iospress.metapress.com/link.asp?id=83968yv8l68253y0
9. McDonald SR et al. "Concurrent administration of coenzyme Q10 and
alpha-tocopherol improves learning in aged mice." Free Radic Biol Med.
38, 6:729-36, 2005.www.elsevier.com
11. Hager K et al. "Alpha-lipoic acid as a new treatment option for
Alzheimer type dementia." Arch Gerontol Geriatr, 32, 3:275-82, 2001.
12. Liu J. “The Effects and Mechanisms of Mitochondrial Nutrient
alpha-Lipoic Acid on Improving Age-Associated Mitochondrial and Cognitive
Dysfunction: An Overview.” Neurochem Res. 2007 Jun 29; Epub ahead of print. http://www.springerlink.com/content/9610161628604736/
18. Schmid-Schonbein, H., Grebe, R., Teitel, P., Artmann, G., Eschweiler, H.,
Schroder, S., "Restoration of microsieve filterability of human red cells
after exposure to hyperosmolarity and lactacidosis: Effect of Vinpocetine",
Drug Development Research, 14, 205-211, 1988. http://www3.interscience.wiley.com/cgi-bin/jhome/34597?CRETRY=1&SRETRY=0
19. Z. Subhan and I. Hindmarch, "Psychopharmacogical Effects of
Vinpocetine in Normal Healthy Volunteers", Eur. J. Clin. Pharmacol.
28, 567-571, 1985. http://www.springerlink.com/content/100413/
21. Grodstein F et al. High-dose antioxidant supplements and cognitive
function in community-dwelling elderly women.” Am J Clin Nutr. 2003
Apr;77(4):975-84. http://www.ajcn.org/cgi/content/full/77/4/975
22. Zhang J et al. “The therapeutic effect of Ginkgo biloba extract in SHR
rats and its possible mechanisms based on cerebral microvascular flow and
vasomotion.” Clin Hemorheol Microcirc. 2000;23(2-4):133-8.
http://iospress.metapress.com/link.asp?id=1rxu2lmw5t9lyyen
23. Walesiuk A et al. "Ginkgo biloba normalizes stress- and
corticosterone-induced impairment of recall in rats." Pharmacol Res.
53, 2:123-8, 2006. www.elsevier.com
24. Walesiuk A et al “Preventive action of Ginkgo biloba in stress- and
corticosterone-induced impairment of spatial memory in rats” Phytomedicine,
May 3, 2007; ePub ahead of print. doi:10.1016/j.phymed.2007.04.012
25. Wang Y et al. "The in vivo synaptic plasticity mechanism of EGb
761-induced enhancement of spatial learning and memory in aged rats." Br
J Pharmacol. 148, 2:147-53, 2006. www.nature.com/bjp
26. Zhang M et al. "Extract of Ginkgo biloba leaves reverses
yohimbine-induced spatial working memory deficit in rats." Behav
Pharmacol. 16, 8:651-6, 2005. www.behaviouralpharm.com
28. Stough C et al. “The chronic effects of an extract of Bacopa monniera
(Brahmi) on cognitive function in healthy human subjects.” Psychopharmacology
(Berl). 2001 Aug;156(4):481-4. http://www.springerlink.com/content/l3yrwct38enavc88/
30. Kishore K and Singh M. “Effect of bacosides, alcoholic extract of Bacopa
monniera Linn. (brahmi), on experimental amnesia in mice.” Indian J Exp
Biol. 2005 Jul;43(7):640-5.
31. Di Iorio A et al. “Markers of inflammation, vitamin E and peripheral
nervous system function: the InCHIANTI study.” Neurobiol Aging. 2006
Sep;27(9):1280-8.
32. Avramovich-Tirosh Y et al. “Neurorescue Activity, APP Regulation and
Amyloid-beta Peptide Reduction by Novel Multi-Functional Brain Permeable Iron-
Chelating- Antioxidants, M-30 and Green Tea Polyphenol, EGCG.” Curr Alzheimer
Res. 2007 Sep;4(4):403-11. http://dx.doi.org/10.2174/156720507781788927
33. Mandel S et al. “Green tea catechins as brain-permeable, natural iron
chelators-antioxidants for the treatment of neurodegenerative disorders.” Mol
Nutr Food Res. 2006 Feb;50(2):229-34. http://www3.interscience.wiley.com/cgi-bin/abstract/112402160
35. Oksman M et al. “Impact of different saturated fatty acid,
polyunsaturated fatty acid and cholesterol containing diets on beta-amyloid
accumulation in APP/PS1 transgenic mice.” Neurobiol Dis. 2006
Sep;23(3):563-72. http://dx.doi.org/10.1016/j.nbd.2006.04.013
36. Green KN et al. “Dietary docosahexaenoic acid and docosapentaenoic acid
ameliorate amyloid-beta and tau pathology via a mechanism involving presenilin 1
levels.” J Neurosci. 2007 Apr 18;27(16):4385-95. http://www.jneurosci.org/cgi/content/short/27/16/4385
37. McCann JC and Ames BN. “Is docosahexaenoic acid, an n-3 long-chain
polyunsaturated fatty acid, required for development of normal brain function?
An overview of evidence from cognitive and behavioral tests in humans and
animals.” Am J Clin Nutr. 2005 Aug;82(2):281-95. http://www.ajcn.org/cgi/content/full/82/2/281
38. Whalley LJ, et al. “Cognitive aging, childhood intelligence, and the
use of food supplements: possible involvement of n-3 fatty acids” AJCN
80,6:1650-57, 2004. www.ajcn.org
39. Freund-Levi Y et al “Omega-3 fatty acid treatment in 174 patients with
mild to moderate Alzheimer disease: OmegAD study: a randomized double-blind
trial” Archives of Neurology 63, 10: 1402- 8, 2006. http://archneur.ama-assn.org/
40. Amenta F et al. “Muscarinic cholinergic receptors in the hippocampus of
aged rats: influence of choline alphoscerate treatment.” Mech Ageing Dev.
1994 Oct 1;76(1):49-64. http://dx.doi.org/10.1016/0047-6374(94)90007-8
41. Aleppo G et al. “Chronic L-alpha-glyceryl-phosphoryl-choline increases
inositol phosphate formation in brain slices and neuronal cultures.” Pharmacol
Toxicol. 1994 Feb;74(2):95-100.
42. Moreno M et al. “Cognitive improvement in mild to moderate Alzheimer's
dementia after treatment with the acetylcholine precursor choline alfoscerate: a
multicenter, double-blind, randomized, placebo-controlled trial.” Clin Ther.
2003 Jan;25(1):178-93. http://dx.doi.org/10.1016/S0149-2918(03)90023-3
43. Secades JJ and Lorenzo JL. “Citicoline: pharmacological and clinical
review, 2006 update.” Methods Find Exp Clin Pharmacol. 2006 Sep;28
Suppl B:1-56. http://journals.prous.com
44. Fioravanti M et al. "Cytidinediphosphocholine CDP-choline for
cognitive and behavioural disturbances associated with chronic cerebral
disorders in the elderly." Cochrane Database Syst Rev. 2:CD000269, 2005. www.mrw.interscience.wiley.com
45. Brown ES et al. “A randomized, placebo-controlled trial of citicoline
add-on therapy in outpatients with bipolar disorder and cocaine dependence.” J
Clin Psychopharmacol. 2007 Oct;27(5):498-502. http://www.psychopharmacology.com/pt/re/jclnpsychopharm
46. Hashioka S et al. “Phosphatidylserine and
phosphatidylcholine-containing liposomes inhibit amyloid beta and
interferon-gamma-induced microglial activation.” Free Radic Biol Med.
2007 Apr 1;42(7):945-54. http://dx.doi.org/10.1016/j.freeradbiomed.2006.12.003
50. Zhou J et al. “Huperzine A attenuates cognitive deficits and
hippocampal neuronal damage after transient global ischemia in gerbils.” Neurosci
Lett. 2001 Nov 9;313(3):137-40. http://dx.doi.org/10.1016/S0304-3940(01)02265-0
51. Lin PY and Su KP. “A meta-analytic review of double-blind,
placebo-controlled trials of antidepressant efficacy of omega-3 fatty acids.” J
Clin Psychiatry. 2007;68(7):1056-61. http://article.psychiatrist.com
52. Lecrubier Y et al. “Efficacy of St. John’s wort extract WS 5570 in
major depression: a double-blind, placebo-controlled trial.” Am J
Psychiatry, 159, 8:1361-6, 2002.
53. Clement K et al. “St. John's wort and the treatment of mild to moderate
depression: a systematic review.” Holist Nurs Pract. 2006
Jul-Aug;20(4):197-203. http://www.hnpjournal.com
54. Woelk H. “Comparison of St John's wort and imipramine for treating
depression: randomised controlled trial.” BMJ. 2000 Sep
2;321(7260):536-9. http://www.bmj.com/cgi/content/full/321/7260/536
55. van Gurp G et al. “St. John’s wort or sertraline? Randomized
controlled trial in primary care.” Can Fam Physician, 48:905-12, 2002.
56. Davidson J et al. “Effect of Hypericum perforatum (St. John’s wort)
in major depressive disorder: a randomized controlled trial.” JAMA,
287, 14:1807-14, 2002.
57. Ham BJ et al. “Decreased GABA levels in anterior cingulate and basal
ganglia in medicated subjects with panic disorder: a proton magnetic resonance
spectroscopy (1H-MRS) study.” Prog Neuropsychopharmacol Biol Psychiatry.
2007 Mar 30;31(2):403-11. http://dx.doi.org/10.1016/j.pnpbp.2006.10.011
60. Lu J and Greco MA. “Sleep circuitry and the hypnotic mechanism of GABAA
drugs.” J Clin Sleep Med. 2006 Apr 15;2(2):S19-26.
61. Deng S et al. “Noni as an anxiolytic and sedative: a mechanism
involving its gamma-aminobutyric acidergic effects.” Phytomedicine.
2007 Aug;14(7-8):517-22. http://dx.doi.org/10.1016/j.phymed.2007.04.005
To a musician, endless days of throbbing masses trigger good times. To a
stressed-out, burned-out average person, continual throbbing masses equal
headaches. These can not only be painful and disruptive, but also destructive to
brain health.
Mark Lubin, chief scientist with RZN Nutraceuticals reported, “Recent
scientific studies at the University of Rochester Medical School have revealed
migraines can actually cause damage to brain cells in a manner extremely similar
to that caused by tiny transient strokes, leaving parts of the brain starved for
oxygen and altering the brain in significant ways.” Thus, he argued, it is
crucial to avoid migraines altogether rather than just fight the pain after it
comes on. “The brain has greatly increased energy demands as it tries to
restore the delicate chemical balance in blood pressure, blood flow, and the
availability of oxygen, nutrients, and waste removal,” he explained, adding a
trigger upsets this balance, sometimes reaching a critical level known as
cortical spreading depression—waves of nerve activity in the smooth muscle
walls of the brain’s micro-vessels that cause contraction and relaxation often
in repeated cycles.
“The herbs used in MIGRA-ZEN RELIEF PLUS (juniper, goldenrod, dandelion,
meadowsweet, willow bark) are known to alter the muscle tone of smooth muscle
tissue, as well as promote reduction of swelling and inflammation.” He
reported a recent a double blind, placebo-controlled clinical study in migraine
patients found in those taking MIGRA-ZEN RELIEF PLUS every day as a preventive,
migraine incidence was reduced by 62.5 percent within seven days, 80 percent
within 14 days, and 100 percent after only 24 days. “This means these patients
ceased to have migraines at all within the indicated time and remained
migraine-free for the remainder of the study,” Lubin explained.
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The
powerful antioxidant coenzyme Q10 (CoQ10) is an important component of the
electron transport chain and, thus, addresses free radicals produced during
oxidative phosphorylation in the inner mitochondrial membrane.5 CoQ10
can be manufactured in the body, but levels decline due to aging; scientists
have found replenishing these levels via CoQ10 supplementation may help stave
off AD, Parkinson’s disease (PD) and other neurodegenerative disorders.6
In 2005, University of Coimbra, Portugal, researchers discovered CoQ10 treatment
in aged, diabetic rats counteracted brain mitochondrial alterations induced by
Abeta1-40 amyloid peptide, suggesting, “CoQ10 therapy can help to avoid a
drastic energy deficiency that characterizes diabetes and Alzheimer’s disease
pathophysiology.”7 Subsequent studies out of Hong Kong confirmed
CoQ10 supplementation protects neuronal cells from amyloid peptide toxicity by
reducing the concentration of superoxideanion.8 Combined
supplementation with CoQ10 and alpha-tocopherols in aged mice improved brain
function, as measured by cognitive tests, according to research from the
University of North Texas, Fort Worth.9